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Journal articles on the topic 'Streptozotocin model'

Author: Grafiati

Published: 28 June 2021

Last updated: 8 February 2022

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1

Skaletskaya, G. N., N. N. Skaletskiy, E. A. Volkova, and V. I. Sevastyanov. "Streptozotocin model of stable diabetes mellitus." Russian Journal of Transplantology and Artificial Organs 20, no. 4 (January 31, 2019): 83–88. http://dx.doi.org/10.15825/1995-1191-2018-4-83-88.

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Aim:to create a model of stable experimental diabetes mellitus (DM) in laboratory rats using streptozotocin (STZ).Materials and methods.The dynamics of changes in glycemia and survival in 60 Wistar rats was determined. STZ at a dosage of 70 mg/kg was administered to these rats in two ways: once and fractionally (within 5 days).Results.After a single injection of the STZ, 6 out of 30 rats (20%) died, in 7 cases (23.3%) a spontaneous reversion of the diabetic status occurred and in 17 animals (56.6%) the DM remained stable throughout the observation period (8 weeks). After the fractional administration of the STZ no mortality was observed. Spontaneous reversal of DM occurred only in 2 of 30 rats (6.6% of cases). In other 28 animals hyperglycemia was stable until the end of the experiment. It is important to note that in all rats with a stable course of DM, the level of glycemia after 2 weeks after the injection of the STZ was at least 20 mmol/l.Conclusion.Fractional intraperitoneal injection of STZ has an obvious advantage compared with a single injection, providing 100% survival and stable course of DM in 93.4%. The main criterion for a stable course of experimental DM is the level of hyperglycemia not less than 20 mmol/l after 2 weeks after intraperitoneal administration of STZ.

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2

Miao, Ming San, Bo Lin Cheng, and Na Jiang. "Effect of Sophora Japonica Total Flavonoids on Mouse Models of Hyperglycemia and Diabetes Model." Applied Mechanics and Materials 664 (October 2014): 397–401. http://dx.doi.org/10.4028/www.scientific.net/amm.664.397.

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Objective: To investigate the effects of Sophora japonica total flavonoids hyperglycemia and diabetes in mice models. Methods: intraperitoneal injection of epinephrine, intravenous injection of freshly prepared alloxan or intravenous injection of streptozotocin, alloxan build adrenaline or hyperglycemia model streptozotocin diabetic model. Glucose values were selected for each experiment> 11.1mmol / L, with a significantly more drinking, eating, and more urinary symptoms in mice 60, according to blood glucose levels were randomly divided into six groups, namely large, medium and small doses of Sophora japonica total flavonoids group, metformin group, the control group and model group. And were fed the appropriate medication, model group and the control group fed with the same volume of saline solution. Results: Sophora japonica total flavonoids can significantly reduce the adrenaline and alloxan mice with high blood sugar glucose levels, improve liver glycogen content; can significantly reduce the streptozotocin-diabetic mouse model of blood glucose levels and improve hepatic glycogen,can significantly improve the streptozotocin-induced islet cell damage. Conclusion: Sophora japonica total flavonoids mouse model of hyperglycemia and diabetes mellitus have a better hypoglycemic effect of its hypoglycemic effect and promote glycogen synthesis, reduce islet cell damage.

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3

Malaisse, Willy J., Marie-Hélène Giroix, Dagmar Zähner, Greta Marynissen, Abdullah Sener, and Bernard Portha. "Neonatal streptozotocin injection: A model of glucotoxicity?" Metabolism 40, no. 10 (October 1991): 1101–5. http://dx.doi.org/10.1016/0026-0495(91)90137-l.

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4

Botolin, Sergiu, and Laura R. McCabe. "Bone Loss and Increased Bone Adiposity in Spontaneous and Pharmacologically Induced Diabetic Mice." Endocrinology 148, no. 1 (January 1, 2007): 198–205. http://dx.doi.org/10.1210/en.2006-1006.

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Insulin-dependent diabetes mellitus (IDDM) is associated with increased risk of osteopenia/osteoporosis in humans. The mechanisms accounting for diabetic bone loss remain unclear. Pharmacologic inducers of IDDM, such as streptozotocin, mimic key aspects of diabetes in rodents, allow analysis at the onset of diabetes, and induce diabetes in genetically modified mice. However, side effects of streptozotocin, unrelated to diabetes, can complicate data interpretation. The nonobese diabetic (NOD) mouse model develops diabetes spontaneously without external influences, negating side effects of inducing agents. Unfortunately, in this model the onset of diabetes is unpredictable, occurs in a minority of male mice, and can only be studied in a single mouse strain. To validate the relevance of the more flexible streptozotocin-induced diabetes model for studying diabetes-associated bone loss, we compared its phenotype to the spontaneously diabetic NOD model. Both models exhibited hyperglycemia and loss of body, fat pad, and muscle weight. Furthermore, these genetically different and distinct models of diabetes induction demonstrated similar bone phenotypes marked by significant trabecular bone loss and increased bone marrow adiposity. Correspondingly, both diabetic models exhibited decreased osteocalcin mRNA and increased adipocyte fatty acid-binding protein 2 mRNA levels in isolated tibias and calvaria. Taken together, multiple streptozotocin injection-induced diabetes is a valid model for understanding the acute and chronic pathophysiologic responses to diabetes and their mechanisms in bone.

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5

GAO, Yu, Jin-hui WU, and Lin LIU. "Streptozotocin-induced early diabetic retinopathy model in rats." Academic Journal of Second Military Medical University 30, no. 10 (December 1, 2010): 1053–59. http://dx.doi.org/10.3724/sp.j.1008.2010.01053.

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6

Mahata, Liganda Endo, Hirowati Ali, and Arina Widya Murni. "Effect of Streptozotocin on Liver Histology Damage in Rats Model of Gestational Diabetes Mellitus." International Journal of Research and Review 8, no. 9 (September 4, 2021): 18–22. http://dx.doi.org/10.52403/ijrr.20210904.

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Background: Gestational Diabetes Mellitus (GDM) is a disorder of carbohydrate metabolism that causes hyperglycemia, insulin resistance and failure of organs especially the liver. There is great interest in understanding the pathophysiology and treatment of GDM. Due to ethical issues involving human studies, it is necessary to use animal models to understand pathophysiology and potential treatment for GDM. Streptozotocin-induced diabetes mellitus in pregnant rats was commonly used by several author. Aims: The aim of this study is to investigate the effect of streptozotocin (STZ) on liver histology in pregnant rats. Methods: Pregnant rats were divided into two groups; 1) Negative control, 2) Positive control. Positive control were pregnant rats induced with a single intraperitoneal injection of streptozotocin 40 mg/Kg b.w. Fourteen days after induction, rats were sacrificed to evaluate the histopathological effect of STZ on the liver using hematoxylin Eosin staining and calculate the presentation of degraded cell and sinusoidal area with ImageJ 1.49v software, National Institute of Health, Bethesda, MD, USA. Data were processed statistically using SPSS with T-Test. Results: Microscopic examination of the liver of STZ-induced rats showed histologic changes in the form of an increase in the number of degenerated cells and a significant expansion of the sinusoidal area (p < 0.000). The percentage of degenerated cells in the healthy group was 9.3%, increased to 70% in the STZ-induced group. In addition, the percentage of the sinusoidal area, which was 19.98% in the healthy group, increased to 49.5%. Conclusions: Streptozotocin induces liver damage in the pregnant rats model. Keywords: Gestational Diabetes Mellitus, Streptozotocin, Liver, Histology

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7

Vastyanov, R. S., and O. V. Chekhlova. "Pathophysiological model of indirect revascularization in rats with microangiopathy of limbs caused by experimental streptozocin diabetes." Reports of Morphology 25, no. 4 (December 19, 2019): 24–29. http://dx.doi.org/10.31393/morphology-journal-2019-25(4)-04.

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Despite the large number of publications, the model of experimental diabetes after the introduction of streptozotocin remains a subject of lively scientific debate. The purpose of this study was to develop a pathophysiological model of indirect revascularization in rats with microangiopathy of limbs caused by experimental streptozotocin diabetes. Experimental studies were carried out in a chronic experiment on 100 sexually mature Wistar rats weighing 180-250 g. The streptozotocin diabetes model used. After culling animals from increased resistance to pancreatotropic toxicity by the criterion of the absence of hyperglycemia, three experimental groups were formed: Group I (control) – rats with streptozotocin-induced angiopathy without treatment (n=10); II group – rats with streptozotocin-induced angiopathy treated with pentoxifylline (100 mg/kg IP for 10 days) for therapeutic purposes (n=25); III group – rats with streptozotocin-induced angiopathy, which together with the treatment were injected with platelet-rich plasma (in the right hind limb, once, with a volume of 0.2 ml, linearly, retrogradely, from two points) and pentoxifylline (100 mg/kg IP for 10 days) (n=25). The duration of the experiment was 110 days. We studied the level of glycemia, the state of microcirculation, and the degree of pathomorphological changes in the various study groups. Statistical processing was performed by non-parametric methods using software Statistica 10.0. The developed pathophysiological model of indirect revascularization with the introduction of pentoxifylline and plasma enriched with platelets in diabetic angiopathy is adequate to the needs of clinical physiology. It has been shown that the isolated administration of pentoxifylline is inferior to combined therapy by revascularizing activity. The results of the work may be an experimental justification for the feasibility of clinical application of the combination of pentoxifylline and platelets rich plasma in the treatment of diabetic angiopathy, as well as its use in prophylactic purposes in patients with diabetes mellitus.

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8

Zhu, Lei, Zhen Zhang, Xiao-jie Hou, Yong-feng Wang, Jing-yu Yang, and Chun-fu Wu. "Inhibition of PDE5 attenuates streptozotocin-induced neuroinflammation and tau hyperphosphorylation in a streptozotocin-treated rat model." Brain Research 1722 (November 2019): 146344. http://dx.doi.org/10.1016/j.brainres.2019.146344.

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9

Gvazava, I. G., A. V. Kosykh, O. S. Rogovaya, O. P. Popova, K. A. Sobyanin, A. K. Khrushchev, A. V. Timofeev, and E. A. Vorotelyak. "A Simplified Streptozotocin-Induced Diabetes Model in Nude Mice." Acta Naturae 12, no. 4 (December 22, 2020): 98–104. http://dx.doi.org/10.32607/actanaturae.11202.

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Preclinical studies of human cellular and tissue-based products (HCT/Ps) for transplantation therapy of type 1 diabetes mellitus (T1DM) necessarily involve animal models, particularly mouse models of diabetes induced by streptozotocin (STZ). These models should mimic the clinical and metabolic manifestations of T1DM in humans (face validity) and be similar to T1DM in terms of the pathogenetic mechanism (construct validity). Furthermore, since HCT/Ps contain human cells, modeling of diabetes in immune-deficient animals is obligatory. Here we describe the most simplified diabetes model in Nude mice. Diabetes was induced in 31 males by a single intraperitoneal injection of STZ in normal saline at a medium-to-high dose of 150 mg/kg body weight. Fourteen control animals received only saline. Non-fasting plasma glucose (PG) levels were measured periodically for 50 days. All STZ-treated mice survived beyond 50 days. By day 15 after STZ administration, 22 of 31 (71%) mice developed stable diabetes based on the following criteria: (1) non-fasting PG 15 mmol/L on consecutive measurements up until day 50; (2) no diabetes remission. The mean non-fasting PG in mice with stable diabetes over the period of 35 days was equal to 25.7 mmol/L. On day 50, mean plasma insulin concentration, mean pancreatic insulin content, and the average number of -cells in pancreatic islets were 2.6, 8.4, and 50 times lower, respectively, than in the control animals. We consider that our Nude mouse model of diabetes meets face validity and construct validity criteria and can be used in preclinical studies of HCT/Ps.

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10

Baig, Mirza Anwar, and Shital Sharad Panchal. "Streptozotocin-Induced Diabetes Mellitus in Neonatal Rats: An Insight into its Applications to Induce Diabetic Complications." Current Diabetes Reviews 16, no. 1 (December 13, 2019): 26–39. http://dx.doi.org/10.2174/1573399815666190411115829.

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Background: Diabetic complications are the major contributor in the mortality of diabetic patients despite controlling blood glucose level. In the journey of new drug discovery, animal models have to play a major role. A large number of chemical-induced and genetically modified animal models have been investigated to induce diabetic complications but none of them was found to be mimicking the pathophysiology of the human. Therefore, the search and identification of the appropriate animal model become essential. Objective: In the present review, we have made an attempt to understand the pathophysiology of diabetic complication in the neonatal streptozotocin-diabetic rat model and tried to identify the targets for therapeutic agents. The review will help the researchers to explore the animal model to induce diabetic complications, to identify targets and further to find lead molecules for treatment or prevention of diabetic complications. Methods: We have compiled the available research work from 1974 by using prominent databases, organized the available information and analyzed the data to improve the understanding of the pathophysiology of streptozotocin-induced diabetic complications in neonates of rats. Results: The neonatal streptozotocin-diabetic rat model is frequently used and well-established animal model for type 2 diabetes mellitus. We have found that this model has been used to study the pathogenesis of various micro and macrovascular diabetic complications and also investigated for its effects on the liver, thymus gland, and brain. The underlying pathophysiology for complications had a resemblance to the human. Conclusion: The neonatal streptozotocin-diabetic rat model may demonstrate symptomatic diabetic complications due to persistent hyperglycemia at the age of approximately 18-24 weeks. Critical interpretations of available research work showed that the researcher can explore split dose STZ (90- 100mg/kg b.w) model to induce Type 2 DM in neonates of rats at 2nd or 3rd postnatal day.

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11

Miao, Ming San, Bo Lin Cheng, Na Jiang, and Mei Qiong Jiang. "Qumai Total Flavonoids Induced Diabetic Mice Model of Streptozotocin." Applied Mechanics and Materials 664 (October 2014): 410–14. http://dx.doi.org/10.4028/www.scientific.net/amm.664.410.

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Purpose: Research Qumai total flavonoids induced diabetic mice model of streptozotocin. Methods: 12 h after fasting groups of mice, Tail vein injection of citrate buffer chain urea with cephalosporins solution (80mg/kg,0.02ml/10g), To 1 times a day. In dosing 10, 20, 30 days tail blood glucose measurement value. On the 30th day fasting 12 h after the last for 1 h, Some blood, Measuring blood glucose、Glycosylation of serum protein, Serum insulin、Insulin resistance value;After the death in mice,Take the liver glycogen original value;Take the pancreas, and kidneys,10% formalin fixed liquid, As a pathological. Results: Compared with model group、blank group, each dose of dianthus superbus flavonoids to chain urea with cephalosporins cause diabetes in mice model can significantly improve the experiment indexes. Conclusion: Dianthus superbus flavonoids to chain urea with cephalosporins caused diabetes in mice model has good therapeutic effect.

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12

Koulmanda, Maria. "Islet transplant model in nonhuman primates: use of streptozotocin." Transplantation Reviews 20, no. 3 (July 2006): 126–30. http://dx.doi.org/10.1016/j.trre.2006.06.003.

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13

Yoshiyama, Yuji, Takashi Sugiyama, and Motoko Kanke. "Experimental Diabetes Model in Chick Embryos Treated with Streptozotocin." Biological & Pharmaceutical Bulletin 28, no. 10 (2005): 1986–88. http://dx.doi.org/10.1248/bpb.28.1986.

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14

Heo, Jae-Hyeok, Kyoung-Min Lee, Sang-Rae Lee, Soon-Tae Lee, Jin-Hwan Oh, Nam-Beom Kim, Kyu-Tae Chang, and Zang-Hee Cho. "P1-123: Streptozotocin-induced Alzheimer model in cynomolgus monkeys." Alzheimer's & Dementia 6 (July 2010): S210. http://dx.doi.org/10.1016/j.jalz.2010.05.672.

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15

Kumar, Anuj, Akhilesh Kumar Rana, Amit Singh, and Alok Singh. "Effect of Methanolic Extract of Phyllanthus niruri on Leptin Level in Animal Model of Diabetes Mellitus." Biomedical and Pharmacology Journal 12, no. 1 (March 27, 2019): 57–63. http://dx.doi.org/10.13005/bpj/1613.

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To study the effect of methanolic extract of Phyllanthus niruri on animal model of Diabetes Mellitus. Diabetes Mellitus was induced in rats by injecting Streptozotocin (60mg/kg) intraperitonealy. Blood glucose was measured on day 3 by GOD-POD method. Rats having fasting blood glucose >250 mg/dl were further selected for study. Four groups were created i.e. Control, Control+Streptozotocin, Streptozotocin+ Metformin(75mg/kg) and Streptozotocin+ extract of P. niruri (250mg/kg). Each group was consisting of 6 rats of either sex. Metformin and experimentalextract were administered for 21 days. Blood Glucose was measured on day 7 and 21. Triglyceride, Cholesterol and Leptin level were also measure by commercially available kit. Anti-oxidant potential was assessed by estimating extent of Lipid peroxidation (LPO) by Malondialdehyde (MDA), Nitric oxide (NO), Superoxide dismutase (SOD) and Glutathione (GSH) in four different tissues i.e. Liver, Kidney, Pancreas, Muscle on day 21. Unpaired and paired student’s t-test were applied for statistical analysis using SPSS Software. The extract of P. niruri showed significant decrease in blood glucose level on day 21 (p-0.04). The treatment didn’t show significant lowering of Leptin and Cholesterol level however Triglyceride level was significantly reduced (p-0.05). The treatment group showed improvement in oxidative stress by increasing SOD and GSH and decreasing LPO and NO activity. The study showed anti-hyperglycemic and anti-oxidative properties of methanolic extract of P.niruri.

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16

Isken, Tonguc, H. Ege Ozgentas, K. Hakan Gulkesen, and Akif Ciftcioglu. "A Random-Pattern Skin-Flap Model in Streptozotocin Diabetic Rats." Annals of Plastic Surgery 57, no. 3 (September 2006): 323–29. http://dx.doi.org/10.1097/01.sap.0000221645.92906.5b.

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17

Gäbel, H., H. Bitter-Suermann, C. Henriksson, J. Säve-Söderbergh, K. Lundholm, and H. Brynger. "Streptozotocin Diabetes in Juvenile Pigs. Evaluation of an Experimental Model." Hormone and Metabolic Research 17, no. 06 (June 1985): 275–80. http://dx.doi.org/10.1055/s-2007-1013518.

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18

Hammad, Samar M., Debra J. Hazen-Martin, Mimi Sohn, Leslie Eldridge, Lyn Powell-Braxton, Wesley Won, and Timothy J. Lyons. "Nephropathy in a Hypercholesterolemic Mouse Model with Streptozotocin-Induced Diabetes." Kidney and Blood Pressure Research 26, no. 5-6 (2003): 351–61. http://dx.doi.org/10.1159/000073942.

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19

Chennasamudram, Sudha P., Shashi Kudugunti, Purushotham Reddy Boreddy, Majid Y. Moridani, and Tetyana L. Vasylyeva. "Renoprotective effects of (+)-catechin in streptozotocin-induced diabetic rat model." Nutrition Research 32, no. 5 (May 2012): 347–56. http://dx.doi.org/10.1016/j.nutres.2012.03.015.

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20

Ghasemi, Asghar, S. Khalifi, and S. Jedi. "Streptozotocin-nicotinamide-induced rat model of type 2 diabetes (review)." Acta Physiologica Hungarica 101, no. 4 (December 2014): 408–20. http://dx.doi.org/10.1556/aphysiol.101.2014.4.2.

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21

Korish, Aida A., Abdel Galil M. Abdel Gader, and Abdulqader A. Alhaider. "Camel milk ameliorates the coagulopathy in streptozotocin diabetic rat model." International Journal of Dairy Technology 68, no. 1 (September 15, 2014): 79–87. http://dx.doi.org/10.1111/1471-0307.12168.

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22

Bailey, L. B., A. Molloy, J. Scott, and D. Rice. "Streptozotocin-induced diabetes is not a model for methylmalonic acidaemia." Journal of Inherited Metabolic Disease 12, no. 4 (December 1989): 429–35. http://dx.doi.org/10.1007/bf01802038.

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23

Ghetia, Sawan Mukund, and Chakrakodi Shashidhara Shastry. "VALIDATION OF DIABETES ASSOCIATED DEPRESSION BY STREPTOZOTOCIN INDUCED RAT MODEL." PLANT ARCHIVES 21, Suppliment-1 (January 15, 2021): 1688–91. http://dx.doi.org/10.51470/plantarchives.2021.v21.s1.266.

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24

Islam, Md Shahidul. "Animal Models of Diabetic Neuropathy: Progress Since 1960s." Journal of Diabetes Research 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/149452.

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Diabetic or peripheral diabetic neuropathy (PDN) is one of the major complications among some other diabetic complications such as diabetic nephropathy, diabetic retinopathy, and diabetic cardiomyopathy. The use of animal models in the research of diabetes and diabetic complications is very common when rats and mice are most commonly used for many reasons. A numbers of animal models of diabetic and PDN have been developed in the last several decades such as streptozotocin-induced diabetic rat models, conventional or genetically modified or high-fat diet-fed C57BL/Ks (db/db) mice models, streptozotocin-induced C57BL6/J and ddY mice models, Chinese hamster neuropathic model, rhesus monkey PDN model, spontaneously diabetic WBN/Kob rat model, L-fucose-induced neropathic rat model, partial sciatic nerve ligated rat model, nonobese diabetic (NOD) mice model, spontaneously induced Ins2 Akita mice model, leptin-deficient (ob/ob) mice model, Otsuka Long-Evans Tokushima Fatty (OLETF) rat model, surgically-induced neuropathic model, and genetically modified Spontaneously Diabetic Torii (SDT) rat model, none of which are without limitations. An animal model of diabetic or PDN should mimic the all major pathogeneses of human diabetic neuropathy. Hence, this review comparatively evaluates the animal models of diabetic and PDN which are developed since 1960s with their advantages and disadvantages to help diabetic research groups in order to more accurately choose an appropriate model to meet their specific research objectives.

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25

Xu, Wenguang, Qiong Luo, Xiuying Wen, Ming Xiao, and Qijian Mei. "Antioxidant and anti-diabetic effects of caffeic acid in a rat model of diabetes." Tropical Journal of Pharmaceutical Research 19, no. 6 (November 13, 2020): 1227–32. http://dx.doi.org/10.4314/tjpr.v19i6.17.

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Purpose: To determine the antioxidant and anti-diabetic potential of a natural flavonoid, caffeic acid in a streptozotocin-induced diabetic rat model.Methods: Experimental diabetes was induced in Wistar rats using streptozotocin injection. Caffeic acid was administered orally on daily basis for 5 weeks. A glucometer was used to monitor fasting blood glucose levels. Insulin levels were estimated using enzyme-linked immunosorbent assay (ELISA). The antioxidant potential of caffeic acid was measured by determining the activities of superoxide dismutase (SOD) and catalase (CAT), and levels of reduced glutathione (GSH) in rat liver. Standard assays were performed to determine the lipid profile of the rats. Histopathological analysis was performed to determine differences in microscopic structures of pancreas among the different treatment groups.Results: Caffeic acid administration resulted in significant enhancement of serum insulin level, and decrease in blood glucose level of diabetic rat models (p < 0.05). Caffeic acid exerted antioxidant effects by significantly increasing GSH levels and activities of CAT and SOD (p < 0.05). Histologicalexamination of the pancreas depicted normal islet morphology under caffeic acid administration in diabetic rats.Conclusion: These results reveal the antioxidant potential and anti-diabetic effect of caffeic acid in a diabetic rat model and point towards the potential applicability of caffeic acid in the management of diabetes mellitus. Keywords: Diabetes mellitus, Streptozotocin, Caffeic acid, Phenolics, Anti-diabetic, Antioxidant

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Yu, Lai-zeng, Xue-peng Zhang, and Ying-xin Wang. "Polygonatum sibiricum extract exerts inhibitory effect on diabetes in a rat model." Tropical Journal of Pharmaceutical Research 18, no. 7 (May 31, 2021): 1493–97. http://dx.doi.org/10.4314/tjpr.v18i7.19.

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Purpose: To investigate the effect of Polygonatum sibiricum extract (PSE) on streptozotocin-induced diabetic rats. Methods: PSE was obtained by steeping the dried Polygonatum sibiricum in water at 60 oC three times, each for 1 h, before first drying in an oven at 100C and then freeze-drying the final extract, thus obtained. Diabetic model rats were prepared by a single intraperitoneal injection of a freshly prepared solution of streptozotocin (50 mg/kg). The rats were randomly divided into 6 groups of ten rats each: negative control, normal control, reference (glibenclamide1 mg/kg) as well as PSE groups, (35, 70 and 140 mg/kg). Blood glucose and plasma insulin levels were measured to determine antihyperglycemic effect. Oxidative stress was evaluated in liver and kidney by their antioxidant markers, viz, lipid peroxidation (LPO), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx) and catalase (CAT). Blood serum levels of creatinine and urea were determined in both diabetic control and treated rats. Results: Compared with diabetic rats, oral administration of PSE at a concentration of 120 mg/kg daily for 30 days showed a significant decrease in fasting blood glucose (118.34 ± 3.29 mg/dL) (p < 0.05) and increased insulin level (12.86± 0.62 uU/mL, p < 0.05). Furthermore, it significantly reduced biochemical parameters (serum creatinine, 0.83 ±0.21 mg/dL, p < 0.05) and serum urea (43.26±1.42 mg/dL, p < 0.05). Conclusion: The results suggest that PSE may effectively normalize impaired antioxidant status in streptozotocin-induced diabetes in a dose-dependent manner. Thus, PSE has a protective effect against lipid peroxidation by scavenging free radicals, restoration of insulin function, and reduction of the incidence of complications.

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27

Ebel, Dalton L., Christopher G. Torkilsen, and Tim D. Ostrowski. "Blunted Respiratory Responses in the Streptozotocin-Induced Alzheimer’s Disease Rat Model." Journal of Alzheimer's Disease 56, no. 3 (February 3, 2017): 1197–211. http://dx.doi.org/10.3233/jad-160974.

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28

Jahr, Henning, Birte Hußmann, Torsten Eckhardt, and Reinhard G. Bretzel. "Successful Single Donor Islet Allotransplantation in the Streptozotocin Diabetes Rat Model." Cell Transplantation 11, no. 6 (September 2002): 513–18. http://dx.doi.org/10.3727/000000002783985576.

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The objective of this study was to define pretransplant islet culture conditions for optimum tissue engraftment in the rat islet allotransplantation model. Lewis rat islets were cultured in TCM 199/5% fetal calf serum for 1 day at 37°C, followed by 1 day of culture at 22°C. When islets from single donors were allotransplanted intraportally into single streptozotocin-diabetic Wistar-Furth rats, complete normoglycemia was restored within 1 day after transplantation in seven out of seven rats, and persisted up to immunological rejection about 1 week later. In five out of six rats receiving a posttransplant injection of antilymphocyte serum, plasma glucose was normalized for >100 days. These data demonstrate, for the first time, successful single-donor-to-single-recipient transplantation of allogeneic rat pancreatic islets. Because islet engraftment may still be regarded as a main problem for clinical islet transplantation, the pretransplant islet culture regimen outlined in this article may lead to a more efficient use of donor pancreatic islet tissue in the clinical setting, as well.

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29

Hamidi, Gholamali, Zohreh Arabpour, Moloud Shabrang, Bahman Rashidi, Hojjatallah Alaei, Mohammad Reza Sharifi, Mahmoud Salami, and Parham Reisi. "Erythropoietin improves spatial learning and memory in streptozotocin model of dementia." Pathophysiology 20, no. 2 (April 2013): 153–58. http://dx.doi.org/10.1016/j.pathophys.2013.01.001.

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30

Baimai, Sani, Phrae Bhanichkul, Passara Lanlua, Apichaya Niyomchan, and Sirinush Sricharoenvej. "Modifications of Adrenal Gland Ultrastructure in Streptozotocin-Induced Diabetic Model Rats." International Journal of Morphology 39, no. 1 (February 2021): 109–15. http://dx.doi.org/10.4067/s0717-95022021000100109.

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31

Wang-Fischer, Yanlin, and Tina Garyantes. "Improving the Reliability and Utility of Streptozotocin-Induced Rat Diabetic Model." Journal of Diabetes Research 2018 (September 23, 2018): 1–14. http://dx.doi.org/10.1155/2018/8054073.

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The Streptozotocin- (STZ-) induced diabetic model is widely used; however, unexplained acute toxicity has given the model an unreliable reputation. To improve the reliability and utility of this model, we characterize the age dependence of STZ toxicity and introduce novel endpoints to assess diabetic complications and reveal possible mechanisms for diabetic development. Diabetes was induced by STZ injection into male, 6 to 23 weeks old, Sprague-Dawley rats. Their metabolic (glucose, lipids, and hormones), inflammatory (cytokines), histologic and behavioral endpoints were observed for 1.2 years. Analgesic compounds were assessed for efficacy treating neuropathy. Acute mortality, within a week of STZ injection (50–65 mg/kg i.v.), was inversely correlated to animal age. Only 3% of rats, age 6–11 weeks, died in the week following STZ injection, whereas 83% of rats 12 to 17 weeks old and 91% of rats 18 weeks or older died in the same week. Partial model recovery (normalized insulin, glucose and food/water intake) was observed starting at week 36; however, pain scores, kidney enlargement, and cataract formation continued to show progression consistent with the diabetic state. Unique noninvasive observational measurements, such as haircoat quality and diarrhea scores, served as useful endpoints for this model. The increased plasma cytokines (such as TNF-α, IL-4, and IL-6) and inflammatory cell infiltration into the pancreatic islets are strong evidence of inflammation in the STZ-induced diabetic model. Pancreatic tissue staining revealed total islet area reduction and confirmed STZ-specific pancreatic toxicity; however, the β-cell density per area in pancreatic islets and insulin levels statistically increased over time in the diabetic rats, suggesting a mechanism for partial recovery of diabetic symptoms. Voltage-gated sodium channel (NaV1.7 specific, peripherally restricted) blocker, CC4148, inhibited neuropathy without side effects as compared to a nonspecific sodium channel inhibitor, Mexiletine, or GABA analog, Pregabalin, which inhibited neuropathy with side effects.

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Klochihina, Ekaterina M., Aleksey K. Erdyakov, Maria P. Morozova, Svetlana A. Gavrilova, Elena S. Akhapkina, Evgeniy V. Ivanov, Zera N. Dzhemilova, et al. "Electrical activity in rat retina in a streptozotocin-induced diabetes model." Diabetes mellitus 21, no. 5 (December 17, 2018): 356–63. http://dx.doi.org/10.14341/dm9490.

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Objectives: Diabetic retinopathy remains the major cause of blindness among the working-age population of developed countries. Considering this, experimental models of diabetes involving laboratory animals are important for assessing clinically significant methods to determine early pathologic alterations of the retina. The early detection of diabetic retinopathy in combination with a search for new pathogenetic targets will enable focusing on new strategies to limit the development of critical changes in the retina and to prolong retinal functioning during the development of diabetes mellitus. Aim: This study aimed to define parameters of electroretinography test that identifies changes due to retinal impairment in diabetes. Methods: Experimental diabetes was induced in Wistar rats by intraperitoneally injecting streptozocin (65 mg/kg; group DM). The control group (CB) received intraperitoneal injections of the vehicle, i.e. citric buffer. On each consecutive day of the experiment, all rats received insulin detemir (2 u/kg). Ophthalmoscopy and electroretinography were conducted before initiating the experiment and after 50, 58 and 66 days of injectin sptreptozocin. Results: Amid 2u\kg insulin injection the glucose level in venous blood in DM group amounted to 30-40 mM. The ophthalmoscopy showed that the optic nerve disk paled by the 50th day, with its line erasing. During electroretinography, wave amplitude in oscillatory potential test tended to decrease. -wave latency of photopic system increased with -wave latency of photopic system and - and -waves latency of scotopic system not altering. In addition, the amplitude of rhythmic stimulation of 8 and 12 Hz decreased. Conclusion: The most apparent parameters of electroretinography for modelling streptozocin-induced diabetes are wave amplitude during the oscillatory potential test, photopic B-wave latency and the amplitude of rhythmic stimulation. These results suggest that in diabetes, ischaemic injury is an important cause of early dysfunction of inner retinal layers.

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高, 逸龙. "Behavioral Abnormalities of Diabetes Mellitus and Streptozotocin-Induced Diabetic Mouse Model." Advances in Clinical Medicine 10, no. 07 (2020): 1348–52. http://dx.doi.org/10.12677/acm.2020.107203.

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Voronkov, D. N., A. V. Stavrovskaya, E. V. Stelmashook, E. E. Genrikhs, and N. K. Isaev. "Neurodegenerative Changes in Rat Brain in Streptozotocin Model of Alzheimer’s Disease." Bulletin of Experimental Biology and Medicine 166, no. 6 (April 2019): 793–96. http://dx.doi.org/10.1007/s10517-019-04442-y.

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35

Ivanov, S. V., R. U. Ostrovskaya, A. V. Sorokina, and S. B. Seredenin. "Analysis of Cytoprotective Properties of Afobazole in Streptozotocin Model of Diabetes." Bulletin of Experimental Biology and Medicine 169, no. 6 (October 2020): 783–86. http://dx.doi.org/10.1007/s10517-020-04978-4.

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Dalli, Tugce, Merve Beker, Sule Terzioglu-Usak, Fahri Akbas, and Birsen Elibol. "Thymoquinone activates MAPK pathway in hippocampus of streptozotocin-treated rat model." Biomedicine & Pharmacotherapy 99 (March 2018): 391–401. http://dx.doi.org/10.1016/j.biopha.2018.01.047.

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37

Johansen, N. J., R. Abela, and J. A. Brock. "Perivascular sympathetic neuropathy in the streptozotocin type I diabetic rat model." Autonomic Neuroscience 163, no. 1-2 (September 2011): 105. http://dx.doi.org/10.1016/j.autneu.2011.05.182.

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dos Santos, João Paulo Almeida, Adriana Fernanda Vizuete, and Carlos-Alberto Gonçalves. "Calcineurin-Mediated Hippocampal Inflammatory Alterations in Streptozotocin-Induced Model of Dementia." Molecular Neurobiology 57, no. 1 (August 6, 2019): 502–12. http://dx.doi.org/10.1007/s12035-019-01718-2.

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39

el-Seifi, S., J. M. Freiberg, J. Kinsella, L. Cheng, and B. Sacktor. "Na+-H+ exchange and Na+-dependent transport systems in streptozotocin diabetic rat kidneys." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 1 (January 1, 1987): R40—R47. http://dx.doi.org/10.1152/ajpregu.1987.252.1.r40.

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The streptozotocin-induced diabetic rat was used to test the hypothesis that Na+-H+ exchange activity in the proximal tubule luminal membrane would be increased in association with renal hypertrophy, altered glomerular hemodynamics, enhanced filtered load and tubular reabsorption of Na+, and stimulated Na+ pump activity in the basolateral membrane, previously reported characteristics of this experimental animal model. Amiloride-sensitive H+ gradient-dependent Na+ uptake and Na+ gradient-dependent H+ flux were increased in brush-border membrane vesicles from the streptozotocin-treated animals. Na+ gradient-dependent uptakes of phosphate, D-glucose, L-proline, and myoinositol were decreased in the drug-induced diabetic animals. These membrane transport alterations were not found when the streptozotocin-diabetic animals were treated with insulin.

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Costa, Virginia Alice Vieira da, and Lucia Marques Vianna. "Biological response of spontaneously hypertensive rats to the streptozotocin administration." Brazilian Archives of Biology and Technology 51, no. 1 (February 2008): 43–48. http://dx.doi.org/10.1590/s1516-89132008000100006.

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The sensitivity of adult spontaneously hypertensive rats (SHR) to the diabetogenic effect of streptozotocin (STZ) was studied. The animals were subdivided into three groups: control (citrate buffer), streptozotocin 40 mg/kg or 50 mg/kg, and general biologic parameters were analyzed, in addition to systolic blood pressure, blood glucose and insulin levels determinations. Both doses were able to induce hyperglycemia above 300 mg/dl; however, 50 mg/kg provoked a more pronounced physiological alterations in body weight, diuresis, water and food intake. There was no change on systolic blood pressure with either dose. Results suggested that SHRs did not need doses of streptozotocin above 40mg/kg in order to produce diabetes probably because this strain was much more sensible than normotensive rats. In addition, streptozotocin might be a drug choice to induce diabetes without provoking alterations in the blood pressure which allowed the use of this experimental model in the studies of induced hypertension-diabetes.

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Hira, Sundas, Uzma Saleem, Fareeha Anwar, Muhammad Farhan Sohail, Zohaib Raza, and Bashir Ahmad. "β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer’s Disease." Biomolecules 9, no. 9 (September 2, 2019): 441. http://dx.doi.org/10.3390/biom9090441.

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Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

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Beebe, LF, and PL Kaye. "Preimplantation development in the streptozotocin-induced diabetic mouse." Reproduction, Fertility and Development 2, no. 4 (1990): 407. http://dx.doi.org/10.1071/rd9900407.

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Streptozotocin (STZ) was used to develop a diabetic mouse model in which to study the development of the preimplantation embryo. STZ doses of 0, 160, 190, 210 and 240 mg kg-1 were given; 190 mg kg-1 was found to be the most suitable as the standard diabetogenic dose, providing about 60% mice with plasma glucose greater than 20 mM. The STZ-diabetic mice responded to superovulation with 10 i.u. of gonadotrophin in the same manner as control mice, producing similar embryo numbers at 48 h, 72 h and 96 h post-hCG. Furthermore, the proportion of 2-cell embryos collected from STZ-diabetic mice which developed to blastocysts in vitro was similar to that of 2-cell embryos from control mice. The STZ-diabetic mouse model after superovulation thus produced normal early preimplantation embryos whose development can be examined in detail in a diabetic environment.

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Hong, Khang Do Gia, Yei-Jin Kang, Ji-Hyeon Oh, Seong-Gon Kim, Young-Wook Park, You-Young Jo, HaeYong Kweon, and Horatiu Rotaru. "The Effect of Sericin on Bone Regeneration in a Streptozotocin-Induced Type I Diabetes Animal Model." Applied Sciences 11, no. 4 (February 3, 2021): 1369. http://dx.doi.org/10.3390/app11041369.

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There is an association between diabetes and impaired bone healing. The purpose of this study was to determine whether sericin had a positive effect on bone regeneration with streptozotocin-induced diabetes in a rat model. Sprague Dawley rats (n = 21) were assigned to one of three groups. A critical-sized bone defect was created on the calvaria. In the sericin group (S group, n = 7), the bone defect was filled with a sericin–gelatin combination, whereas in the gelatin group (G group, n = 7), only gelatin sponge was used. The control group (N group, n = 7) did not receive any graft. New bone formation was evaluated by micro-computerized tomogram and histological analysis. The regenerated bone volume in group S was the highest among the three groups (3.87 ± 2.51 mm3), followed by group N (1.71 ± 1.65 mm3) and group G (1.24 ± 1.05 mm3). The application of sericin in combination with a gelatin sponge enhanced the process of bone regeneration in streptozotocin-induced type I diabetes animal model.

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Kirkham, D. M., G. J. Murphy, and P. Young. "Demonstration of inhibitory guanine nucleotide regulatory protein (Gi) function in liver and hepatocyte membranes from streptozotocin-treated rats." Biochemical Journal 284, no. 2 (June 1, 1992): 301–4. http://dx.doi.org/10.1042/bj2840301.

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By using a defined plasma-membrane preparation, functional inhibition of adenylate cyclase activity by the inhibitory G-protein (Gi) was observed in liver and hepatocyte membranes from rats made diabetic by streptozotocin. These observations contrast with previous reports which have shown a defect in Gi in this diabetic animal model. These results suggest that Gi function is not impaired in the livers of streptozotocin-treated rats and that plasma-membrane preparation procedures should be clearly defined before ascribing Gi defects to a pathological state such as diabetes.

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Lester-Coll, Nataniel, Enrique J. Rivera, Stephanie J. Soscia, Kathryn Doiron, Jack R. Wands, and Suzanne M. de la Monte. "Intracerebral streptozotocin model of type 3 diabetes: Relevance to sporadic Alzheimer's disease." Journal of Alzheimer's Disease 9, no. 1 (April 6, 2006): 13–33. http://dx.doi.org/10.3233/jad-2006-9102.

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Wilson, Rachel D., and Md Shahidul Islam. "Fructose-fed streptozotocin-injected rat: an alternative model for type 2 diabetes." Pharmacological Reports 64, no. 1 (January 2012): 129–39. http://dx.doi.org/10.1016/s1734-1140(12)70739-9.

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Lee, Hong-Joo, Kyung Hwan Jeong, Yang Gyun Kim, Joo Young Moon, Sang Ho Lee, Chun Gyoo Ihm, Ji Youn Sung, and Tae Won Lee. "Febuxostat Ameliorates Diabetic Renal Injury in a Streptozotocin-Induced Diabetic Rat Model." American Journal of Nephrology 40, no. 1 (2014): 56–63. http://dx.doi.org/10.1159/000363421.

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Filho, Omar Andrade Rodrigues, and Valéria Paula Sassoli Fazan. "Streptozotocin induced diabetes as a model of phrenic nerve neuropathy in rats." Journal of Neuroscience Methods 151, no. 2 (March 2006): 131–38. http://dx.doi.org/10.1016/j.jneumeth.2005.06.024.

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Estil·les, Elisabet, Noèlia Téllez, Montserrat Nacher, and Eduard Montanya. "A Model for Human Islet Transplantation to Immunodeficient Streptozotocin-Induced Diabetic Mice." Cell Transplantation 27, no. 11 (October 1, 2018): 1684–91. http://dx.doi.org/10.1177/0963689718801006.

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Streptozotocin (STZ) is a cytotoxic glucose analogue that causes beta cell death and is widely used to induce experimental diabetes in rodents. The sensitivity of beta cells to STZ is species-specific and human beta cells are resistant to STZ. In experimental islet transplantation to rodents, STZ-diabetes must be induced before transplantation to avoid destruction of grafted islets by STZ. In human islet transplantation, injection of STZ before transplantation is inconvenient and costly, since human islet availability depends on organ donation and frail STZ-diabetic mice must be kept for unpredictable lapses of time until a human islet preparation is available. Based on the high resistance of human beta cells to STZ, we have tested a new model for STZ-diabetes induction in which STZ is injected after human islet transplantation. Human and mouse islets were transplanted under the kidney capsule of athymic nude mice, and 10–14 days after transplantation mice were intraperitoneally injected with five consecutive daily doses of STZ or vehicle. Beta-cell death increased and beta-cell mass was reduced in mouse islet grafts after STZ injection. In contrast, in human islet grafts beta cell death and mass did not change after STZ injection. Mice transplanted with rodent islets developed hyperglycemia after STZ-injection. Mice transplanted with human islets remained normoglycemic and developed hyperglycemia when the graft was harvested. STZ had no detectable toxic effects on beta cell death, mass and function of human transplanted islets. We provide a new, more convenient and cost-saving model for human islet transplantation to STZ-diabetic recipients in which STZ is injected after islet transplantation.

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Zhou, Xiang, Yu Feng, Zhoubing Zhan, and Jianchang Chen. "Hydrogen Sulfide Alleviates Diabetic Nephropathy in a Streptozotocin-induced Diabetic Rat Model." Journal of Biological Chemistry 289, no. 42 (August 27, 2014): 28827–34. http://dx.doi.org/10.1074/jbc.m114.596593.

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