Gotowe bibliografie tematyczne / HepG2 cells

Gotowa bibliografia na temat „HepG2 cells”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "HepG2 cells"

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Sary, Hanan G., Nahla A. Ayoub, Abdel Nasser B. Singab, Mickey Vinodh i Khaled Y. Orabi. "ISOLATION OF BIOACTIVE COMPOUNDS FROM CENTAUREA AEGYPTIACA". International Journal of Pharmacy and Pharmaceutical Sciences 10, nr 4 (1.04.2018): 1. http://dx.doi.org/10.22159/ijpps.2018v10i4.17528.

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Objective: In a previous study, Centaurea aegyptiaca ethanol and ethyl acetate extracts showed potent cytotoxic effects against laryngeal (HEP2) and hepatic (HEPG2) carcinoma cell lines. Additionally, two novel compounds were isolated and identified. The aim of this study is to continue isolating and identifying another compound (s) that may, also, be responsible for this potent biological activity.Methods: C. aegyptiaca dried aerial parts were extracted with ethanol and ethyl acetate. Both extracts were chromatographed separately to afford seven guaianolides that were identified using different spectroscopic methods. Moreover, compounds 1-7 were evaluated for their cytotoxicity (IC50, µM) against HEP2 and HEPG2 cells in comparison to the normal fibroblasts (BHK) using sulforhodamine B assay. Doxorubicin was used as a positive control.Results: Seven sesquiterpene lactones, centaurepensin, also known as chlorohyssopifolin A (1), 8α-hydroxy-11α, 13-dihydrozaluzanin C (2), chlorohyssopifolin B (3), desacylcynaropicrin (4), chlorohyssopifolin C, acroptilin (5), subluteolide (6), and solstitiolide (7) were isolated from C. aegyptiaca extracts and identified. This is the first report on the occurrence of 2, 4, 5 and 6 in C. aegyptiaca. Compounds 1-4 and 6 exhibited selective cytotoxic effects against HEP2 and HEPG2 cells. However, compounds 1 and 7 showed the highest activities against HEP2 with IC50 values of 10.6±0.02 and 10.9±0.03 µM, respectively. Moreover, compound 3 was the most potent one against HEPG2 cells with IC50value of 13.8±0.05 µM.Conclusions: Chemical investigation of C. aegyptiaca ethanol and ethyl acetate extracts led to the isolation and identification of seven guaianolides. These compounds exhibited good cytotoxic activities against HEP2 and HEPG2 cell lines.
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Pang, Ye-Bin, Jian He, Bi-Yu Cui, Sheng Xu, Xi-Lei Li, Man-Ya Wu, Rong Liang i in. "A Potential Antitumor Effect of Dendritic Cells Fused with Cancer Stem Cells in Hepatocellular Carcinoma". Stem Cells International 2019 (1.04.2019): 1–10. http://dx.doi.org/10.1155/2019/5680327.

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HCC stem cells were reported as posttreatment residual tumor cells that play a pivotal role in tumor relapse. Fusing dendritic cells (DCs) with tumor cells represents an ideal approach to effectively activate the antitumor immunity in vivo. DC/HCC stem cell vaccine provides a potential strategy to generate polyclonal immune response to multiple tumor stem cell antigens including those yet to be unidentified. To assess the potential capacity of DC/HCC stem cell vaccines against HCC, CD90+HepG2 cells were sorted from the HCC cell line HepG2. DC and CD90+HepG2 and DC and HepG2 fused cells were induced by polyethylene glycol (PEG). The influence of fusion cells on proliferation and immunological function transformation of lymphocytes was assessed by FCM and ELISA assay, respectively. The cytotoxicity assay of specific fusion cell-induced CTLs against HepG2 was conducted by CytoTox 96 Non-Radioactive Cytotoxicity Assay kit in vitro. At last, the prevention of HCC formation in vivo was described in a mouse model. The results of FCM analysis showed that the proportion of CD90+HepG2 cells in the spheral CD90+HepG2 enriched by suspension sphere culture was ranging from 98.7% to 99.5%, and 57.1% CD90+HepG2/DC fused cells were successfully constructed. The fusion cells expressed a higher level of costimulatory molecules CD80, CD83, CD86, and MHC-I and MHC-II molecules HLA-ABC and HLA-DR than did immature DCs (P<0.05). And the functional analysis of fusion cell-induced CTLs also illustrated that CD90+HepG2/DC fusion cells showed a greater capacity to activate proliferation of lymphocytes in vitro (P<0.05). The CD90+HepG2/DC-activated CTLs had a specific killing ability against CD90+HepG2 cells in vivo. These results suggested that CD90+HepG2/DC fusion cells could efficiently stimulate T lymphocytes to generate specific CTLs targeting CD90+HepG2 cells. It might be a promising strategy of immunotherapy for HCC.
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Choi, Hyo-Kyoung, i Min-Yu Chung. "Isoeugenol Inhibits PCSK9 in HepG2 Cells". Journal of the Korean Society of Food Science and Nutrition 49, nr 9 (30.09.2020): 919–24. http://dx.doi.org/10.3746/jkfn.2020.49.9.919.

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Lee, Junmin, Aly Ung, Hanjun Kim, KangJu Lee, Hyun-Jong Cho, Praveen Bandaru, Samad Ahadian, Mehmet R. Dokmeci i Ali Khademhosseini. "Engineering liver microtissues to study the fusion of HepG2 with mesenchymal stem cells and invasive potential of fused cells". Biofabrication 14, nr 1 (30.11.2021): 014104. http://dx.doi.org/10.1088/1758-5090/ac36de.

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Abstract Increasing evidence from cancer cell fusion with different cell types in the tumor microenvironment has suggested a probable mechanism for how metastasis-initiating cells could be generated in tumors. Although human mesenchymal stem cells (hMSCs) have been known as promising candidates to create hybrid cells with cancer cells, the role of hMSCs in fusion with cancer cells is still controversial. Here, we fabricated a liver-on-a-chip platform to monitor the fusion of liver hepatocellular cells (HepG2) with hMSCs and study their invasive potential. We demonstrated that hMSCs might play dual roles in HepG2 spheroids. The analysis of tumor growth with different fractions of hMSCs in HepG2 spheroids revealed hMSCs’ role in preventing HepG2 growth and proliferation, while the hMSCs presented in the HepG2 spheroids led to the generation of HepG2-hMSC hybrid cells with much higher invasiveness compared to HepG2. These invasive HepG2-hMSC hybrid cells expressed high levels of markers associated with stemness, proliferation, epithelial to mesenchymal transition, and matrix deposition, which corresponded to the expression of these markers for hMSCs escaping from hMSC spheroids. In addition, these fused cells were responsible for collective invasion following HepG2 by depositing Collagen I and Fibronectin in their surrounding microenvironment. Furthermore, we showed that hepatic stellate cells (HSCs) could also be fused with HepG2, and the HepG2-HSC hybrid cells possessed similar features to those from HepG2-hMSC fusion. This fusion of HepG2 with liver-resident HSCs may propose a new potential mechanism of hepatic cancer metastasis.
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Zhou, Shuping, Yongfang Ma, Xueke Liu, Pan Yu, Ning Huang, Li Song, Ruyue Xu, Zhen Huo, Tao Zhu i Xiaolong Tang. "Targeted Delivery of Glypican 3 (GPC3) Antibody-Modified MicroRNA (miR let-7b-5p) Polymer Nanoparticles to Sorafenib-Resistant Hepatsocellular Carcinoma Cells". Journal of Biomedical Nanotechnology 17, nr 4 (1.04.2021): 677–90. http://dx.doi.org/10.1166/jbn.2021.3033.

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The miR let-7b-5p (a kind of microRNAs) has many pathophysiological regulation effects, including human hepatocellular carcinoma (HCC) pathogenesis. This study investigated whether nanoparticle-mediated miR let-7b-5p could jointly enhance the therapeutic effect of sorafenib on HCC by inhibiting the proliferation of HCC cells, inducing apoptosis, and reversing drug resistance. We evaluated the level of miR let-7b-5p in sorafenib-resistant HepG2 cells (HepG2R) and HepG2 HCC cells by qRT-PCR and analyzed the biological effects of hepatocellular carcinoma treated with sorafenib with miR let-7b-5p, and further studied the toxicity of nanoparticles (Ab-miR-NPs) that deliver miR let-7b-5p mimics and target GPC3 on the surface of hepatocellular carcinoma cells. Results showed that, in HepG2 cells, the expression level of miR let-7b-5p was significantly higher than that in HepG2R cells. Targeted nanoparticle Ab-miR-NPs mediated the delivery of miR let-7b-5p to the HCC cytoplasm and released miRNA after being broken down, down-regulating the expression of IGF1R and inhibiting AKT/mTOR and Ras/Raf signal transmission. Ab-miR-NPs not only enhanced the proliferation of sorafenib in cultured HepG2R cells and induced cell apoptosis efficiency, but they also improved the anti-tumor activity in the mouse models. These results indicated that GPC3 antibody-modified PLGA-PLL (polylactic acid-glycolic acetic copolymer grafted hyper-branched polylysine) loaded miR let-7b-5p polymer nanoparticles combined with sorafenib may be a new treatment strategy for HCC resistant to sorafenib.
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Chang, Xiaomin, Xuerong Zhao, Jianping Wang, Shi Ding, Lijun Xiao, Enhong Zhao i Xin Zheng. "Effect of Hsp90 Inhibitor KW-2478 on HepG2 Cells". Anti-Cancer Agents in Medicinal Chemistry 19, nr 18 (7.02.2020): 2231–42. http://dx.doi.org/10.2174/1871520619666191023094610.

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Objective: The objectives of this study were to investigate the effects of proliferation, apoptosis, cell cycle, invasion, and senescence of KW-2478 on HepG2 cells, and to explore the related mechanism of apoptosis and the cell cycle. Methods: HepG2 cells (hepatocellular carcinoma cells) were cultured with KW-2478, at different doses and for different times, in vitro. The MTT assay was used to detect the effect of KW-2478 on proliferation of HepG2 cells. Flow cytometry was used to determine the effects of KW-2478 on the cell cycle and apoptosis of HepG2 cells. The Transwell assay was used to determine the effect of KW-2478 on cell invasion. The β-galactosidase assay tested the effect of low-dose KW-2478 on the senescence of HepG2 cells. Western blotting and the quantitative polymerase chain reaction were used respectively to assess changes in protein and mRNA levels of related factors in HepG2 cells after the KW-2478 treatment. Results: KW-2478 significantly inhibited proliferation of HepG2 cells. KW-2478 induced apoptosis and cell cycle arrest of HepG2 cells, and inhibited the invasion of HepG2 cells; low dose KW-2478 promoted HepG2 senescence. Conclusions: KW-2478 inhibited the proliferation of HepG2 cells, induced apoptosis and cell cycle arrest, inhibited invasion, and promoted senescence. KW-2478 affected the expression of related factors in the mitochondrial apoptotic signaling and cell cycle-related regulatory pathways. KW-2478 downregulated the expression of STAT3, which is a key factor in the JAK-STAT pathway, indicating that KW-2478 may affect the function of HepG2 cells by downregulating STAT3.
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Abdel Aziz, Mohamed Talaat, Hussien Mostafa Khaled, Ali El Hindawi, Nagwa Kamal Roshdy, Laila A. Rashed, Dina Sabry, Amira A. Hassouna, Fatma Taha i Walaa Ibrahim Ali. "Effect of Mesenchymal Stem Cells and a Novel Curcumin Derivative on Notch1 Signaling in Hepatoma Cell Line". BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/129629.

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This study was conducted to evaluate the effect of mesenchymal stem cells (MSCs) and a novel curcumin derivative (NCD) on HepG2 cells (hepatoma cell line) and to investigate their effect on Notch1 signaling pathway target genes. HepG2 cells were divided into HepG2 control group, HepG2 cells treated with MSC conditioned medium (MSCs CM), HepG2 cells treated with a NCD, HepG2 cells treated with MSCs CM and NCD, and HepG2 cells treated with MSCs CM (CM of MSCs pretreated with a NCD). Expression of Notch1, Hes1, VEGF, and cyclin D1 was assessed by real-time, reverse transcription-polymerase chain reaction (RT-PCR) in HepG2 cells. In addition, HepG2 proliferation assay was performed in all groups. Notch1 and its target genes (Hes1 and cyclin D1) were downregulated in all treated groups with more suppressive effect in the groups treated with both MSCs and NCD. Also, treated HepG2 cells showed significant decrease in cell proliferation rate. These data suggest that modulation of Notch1 signaling pathway by MSCs and/or NCD can be considered as a therapeutic target in HCC.
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Negoro, Ryosuke, Mitsuki Tasaka, Sayaka Deguchi, Kazuo Takayama i Takuya Fujita. "Generation of HepG2 Cells with High Expression of Multiple Drug-Metabolizing Enzymes for Drug Discovery Research Using a PITCh System". Cells 11, nr 10 (18.05.2022): 1677. http://dx.doi.org/10.3390/cells11101677.

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HepG2 cells are an inexpensive hepatocyte model that can be used for repeated experiments, but HepG2 cells do not express major cytochrome P450s (CYPs) and UDP glucuronosyltransferase family 1 member A1 (UGT1A1). In this study, we established CYP3A4–POR–UGT1A1–CYP1A2–CYP2C19–CYP2C9–CYP2D6 (CYPs–UGT1A1) knock-in (KI)-HepG2 cells using a PITCh system to evaluate whether they could be a new hepatocyte model for pharmaceutical studies. To evaluate whether CYPs–UGT1A1 KI-HepG2 cells express and function with CYPs and UGT1A1, gene expression levels of CYPs and UGT1A1 were analyzed by using real-time PCR, and metabolites of CYPs or UGT1A1 substrates were quantified by HPLC. The expression levels of CYPs and UGT1A1 in the CYPs–UGT1A1 KI-HepG2 cells were comparable to those in primary human hepatocytes (PHHs) cultured for 48 h. The CYPs and UGT1A1 activity levels in the CYPs–UGT1A1 KI-HepG2 cells were much higher than those in the wild-type (WT)-HepG2 cells. These results suggest that the CYPs–UGT1A1 KI-HepG2 cells expressed functional CYPs and UGT1A1. We also confirmed that the CYPs–UGT1A1 KI-HepG2 cells were more sensitive to drug-induced liver toxicity than the WT-HepG2 cells. CYPs–UGT1A1 KI-HepG2 cells could be used to predict drug metabolism and drug-induced liver toxicity, and they promise to be a helpful new hepatocyte model for drug discovery research.
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Tian, Sha, Zhuo Liu, Qing Zhou, Ruoxia Wu, Xiaodi Huang, Zicheng Liang, Zhen Zhang i Xuefei Tian. "Upregulation of MiR-340-5p Reverses Cisplatin Sensitivity by Inhibiting the Expression of CDK6 in HepG2 Cells". Folia Biologica 69, nr 2 (13.07.2021): 57–66. http://dx.doi.org/10.3409/fb_69-2.08.

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Cisplatin (CDDP) has been successfully used in chemotherapy for liver cancer. However, the development of CDDP resistance in HepG2 cells usually leads to relapse and a worsening prognosis. MiR-340-5p has attracted much attention because of its ability to affect cell resistance. This project is intended to explore the role of miR-340-5p and CDK6 in CDDP-R HepG2 cells and provide new ideas for the treatment of liver cancer. A dual-luciferase reporter assay was used to confirm the targeting relationship between miR-340-5p and CDK6. We constructed a CDDP-resistant model of HepG2 cells to examine the effect of miR-340-5p on the drug sensitivity of HepG2 cells. CDDP-R HepG2 cells were transfected with miR-340-5p overexpression plasmid and CDK6 silencing plasmid. QRT-PCR was used to detect the expression of miR-340-5p and CDK6. A western blot was performed to determine the expression of CDK6, CyclinD1, and CyclinD2. CCK-8, flow cytometry, TUNEL and Clonogenic assays were also carried out to detect CDDP-R HepG2 cells. There is a targeting relationship between miR-340-5p and CDK6. The drug resistance of CDDP-R HepG2 cells was significantly higher than that of CDDP-S HepG2 cells. CDDP-R HepG2 cells transfected with both miR-340-5p overexpressing plasmid and CDK6 silencing plasmid showed a lower proliferation ability, cell cycle arrest in the G0/G1 phase, and lower drug resistance compared with single CDDP-R HepG2 cells. Overexpression of miR-340-5p aggravated CDDP-R HepG2 cells' apoptosis and inhibited cell viability. Overexpression of miR-340-5p could reverse the sensitivity of HepG2 cells to CDDP by inhibiting the expression of CDK6 in HepG2 cells.
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Alburae, Najla Ali, i Afrah Eltayeb Mohammed. "Antiproliferative effect of the Red Sea cone snail, Conus geographus". Tropical Journal of Pharmaceutical Research 19, nr 3 (9.04.2020): 577–81. http://dx.doi.org/10.4314/tjpr.v19i3.17.

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Purpose: To investigate the antiproliferative effect of the Red Sea cone snail, Conus geographus, against 4 MCF-7 (breast), MDA-MB-231 (epithelial human breast), HepG2 (hepatocellular) and SKOV-3 (ovarian) cancer cell lines. Methods: Extraction of Red Sea cone snail sample with a mixture of CH2Cl2 and CH3OH (1:1, v/v) yielded 0.55 g of a green viscous material. The cytotoxic effects of the organic extract against the cancer cell lines were determined using cell proliferation (MTT) assay, and the half-maximal concentration (IC50) values measured. The effect of the crude extract on the cell cycle of the HepG-2 was determined by flow cytometry. Results: The extract produced significant inhibitory effects against SKOV-3, MDA-MB-231, MCF-7 and HepG2, with IC50 values of 22.7 ± 2.2, 68.7 ± 6.2, 47 ± 4.2 and 19 ± 2.1 μg/mL, respectively. Cell cycle analysis revealed that the extract enhanced accumulation of HepG2 cells in the Go/G1 phase, at a level of 23.4 and 24.1 % at IC50 (19 μg/mL) and ½ IC50 (9.5 μg/mL), respectively, when compared to the untreated cells. Conclusion: These results indicate that C. geographus extract exhibits potent cytotoxic effect against HepG2 cells via a mechanism involving G0/G1 cell cycle arrest. Thus, C. geographus is a potential source of a new anti-cancer agent. Keywords: Conus geographus, Marine invertebrate, HepG2, Antiproliferation
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Rozprawy doktorskie na temat "HepG2 cells"

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呂可欣 i Ho-yan Lui. "Effects of lipoic acid on oxidant-induced cytotoxicity in HepG2 cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969768.

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Lui, Ho-yan. "Effects of lipoic acid on oxidant-induced cytotoxicity in HepG2 cells". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2203240X.

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Vahdati-Mashhadian, Nasser. "Regulation of CYP3A gene expression in human HepG2 hepatoma cells". Thesis, University of Surrey, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364817.

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Colton, Heidi Muth. "Dissecting Mechanisms of Toxicity in HepG2 Cells Using Gene Expression Analysis". NCSU, 2002. http://www.lib.ncsu.edu/theses/available/etd-09132002-161850/.

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Reduction/oxidation (redox) balance is a critical component of cell viability. When oxidants reach levels that overcome the ability of antioxidants to eliminate them, it results in damage to cellular macromolecules. The damage to DNA, lipids and protein initiates a cascade of physiological events in response to the oxidative stress. Researchers have been studying these cellular responses by analyzing gene expression and protein activity for many years. Recently, new technologies have emerged that allow scientists to analyze the differential expression of extremely large sets of genes in response to oxidative stressors and other toxicants. Most experiments performed to date have involved a single dose of a chemical and a single timepoint for analysis. However, gene expression has proven to be a dynamic process with many transcriptional changes over a relatively short timecourse. In order to study the dynamic nature of gene expression and its effects on cellular physiology, experiments were performed to analyze the effects of oxidative stress on HepG2 cells over a 24 hour timecourse with a range of doses of the glutathione depletor, diethylmaleate (DEM). Using Clontech microarrays, TaqMan RT-PCR, and assays to measure reduced glutathione (GSH) concentrations and to determine cell cycle status, an overall picture of the effects of oxidative stress in relation to dose and time was created. DEM caused GSH depletion to the extent that cells treated with 1.25mM DEM for 4 hours contained less than 20% of the GSH levels in untreated cells. The redox imbalance caused the transcription of genes that initiate cell cycle arrest, DNA repair, and induction of stress proteins. The p53-independent induction of p21 initiated a cascade of events including the decreased transcription of cyclins that resulted in cell cycle arrest. Additionally, the transcription of stress induced genes such as HSP70 and heme oxygenase-1 exhibited significant time and dose-dependent increases in reponse to DEM. While the genes exhibiting differential expression remained generally the same between doses, it was the time taken for these gene changes to occur that varied greatly from the highest dose to the lowest dose of DEM. These experiments demonstrate the importance of analyzing an effective dose range over an extended time period when using differential gene expression to study the mechanisms of toxicity.
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Etwebi, Zienab. "Magnesium Regulation of Glucose and Fatty Acid Metabolism in HEPG2 Cells". Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1307564164.

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Wang, Hui. "Molecular mechanisms of oridonin-induced cytotoxicity and apoptosis in HepG2 cells". HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1162.

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Syed, Noor Afshan. "Regulation of glycogen synthase and glycogen phosphorylase by insulin in HepG2 cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63926.pdf.

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Portolesi, Roxanne, i roxanne portolesi@flinders edu au. "Fatty acid metabolism in HepG2 cells: Limitations in the accumulation of docosahexaenoic acid in cell membranes". Flinders University. Medicine, 2007. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20070802.103146.

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The current dietary recommendations for optimal health are designed to increase our intake of two bioactive omega-3 (n-3) fatty acids, eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3), abundant naturally in fatty fish such as salmon. Health authorities recommend that the general population consume two to three fatty fish meals per week (1) for optimal health and for the prevention of cardiovascular disease. However, some modern Western societies consume only modest amounts of fish and seafood (2;3). Land based vegetable oils may provide an alternative to meet these needs. Linseed and canola oils are rich in alpha-linolenic acid (ALA, 18:3n-3) (4). ALA can be converted endogenously to EPA and DHA and suggests that increasing the dietary intake of ALA may increase the conversion and accumulation of DHA in tissues and plasma. However, elevated dietary intakes of ALA in animals and humans results in an increased level of EPA in tissues yet there is little or no change in the level of DHA (5-7). The current consensus is that the synthesis of DHA from ALA in humans is limited yet the mechanisms involved in regulating the accumulation of DHA in tissues are poorly understood. The reputed rate-limiting enzyme in the conversion of fatty acids is delta 6 desaturase (D6D). ALA is a substrate for D6D and undergoes a series of desaturation and elongation reactions to yield n-3 long chain polyunsaturated fatty acids (LCPUFA). The final step in the synthesis of DHA from ALA involves translocation of its immediate fatty acid precursor, 24:6n-3 from the endoplasmic reticulum to the peroxisome to be partially beta-oxidised to yield DHA. The involvement of multiple enzymes in the desaturation-elongation pathway, and the integration of other pathways, such as phospholipid biosynthesis, suggests there are various steps that may regulate the accumulation of DHA in cell membranes. This thesis aimed to examine the possible regulatory steps in the conversion of fatty acids to LCPUFA, particularly in the synthesis of DHA from n-3 fatty acid precursors. The human hepatoma cell line, HepG2, was used as an in vitro cell system to examine the accumulation of individual fatty acids and their metabolites in isolation from other competing fatty acid substrates. The accumulation of linoleic acid (LA, 18:2n-6) and ALA in HepG2 cell phospholipids following supplementation with increasing concentrations of each respective fatty acid correlated with that described in vivo, as was the accumulation of their conversion products. The accumulation of DHA in cells supplemented with ALA reached a plateau at concentrations above 5 micro g/ml and paralleled the accumulation of 24:6n-3 in cell phospholipids, suggesting that the delta 6 desaturation of 24:6n-3 was prevented by increasing concentrations of ALA, thereby limiting the accumulation of DHA. The accumulation of DHA in cells supplemented with eicosapentaenoic acid (EPA, 20:5n-3) or docosapentaenoic acid (DPA, 22:5n-3) was significantly greater than the level of DHA that accumulated in cells supplemented with ALA. However, regardless of substrate, the level of DHA in cell membranes reached a plateau at substrate concentrations above 5 micro g/ml. This thesis further aimed to examine the effect of fatty acid supplementation on the mRNA expression of D6D in HepG2 cells. The expression and activity of D6D mRNA is subject to nutritional and hormonal regulation. The mRNA expression of D6D in HepG2 cells following supplementation with oleic acid (OA, 18:1n-9), LA, ALA, arachidonic acid (AA, 20:4n-6) or EPA was examined by real time RT PCR. The expression of D6D mRNA was reduced by up to 50% in cells supplemented with OA, LA, ALA , AA or EPA compared with control cells and suggests that fatty acids modulate the expression of the key enzyme involved in the conversion of fatty acids. The effect of fatty acid co-supplementation on the fatty acid composition of HepG2 cell phospholipids was also examined in an attempt to gain insights into the role of D6D and the enzymes involved in peroxisomal beta-oxidation on the accumulation of DHA from n-3 fatty acid precursors. The reduction in the accumulation of DHA in cells co-supplemented with DPA and docosatetraenoic acid (DTA, 22:4n-6) was greater than in cells co-supplemented with DPA and LA, suggesting that peroxisomal beta-oxidation may have a greater role in determining the accumulation of DHA from DPA than the activity of D6D. Further investigation should be directed towards understanding the role that peroxisomal beta-oxidation may play in the synthesis of DHA from precursor fatty acids. The fatty acid composition of cell membranes in vivo is a result of several physiological processes including dietary intake, phospholipids biosynthesis and fatty acid conversion as well as catabolic processes. This thesis demonstrates that a greater understanding of the regulation of the conversion of fatty acids will help to define dietary approaches that enhance the synthesis of n-3 LCPUFA from n-3 fatty acid precursors to lead to improved outcomes for health.
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Morton, Latarchal D. "Ceramide stimulates 3 -methylcholanthrene’s ability to induce cytochrome (cyp1a1) p450 in hepg2 cells". DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2005. http://digitalcommons.auctr.edu/dissertations/3648.

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This study showed that dihydroceramide and ceramide increased the expression of cytochrome (CYP) P450 when HepG2 cells were exposed to 3-methylcholanthrene (MC). Cytochrome P450s are a highly diversified set of heme proteins responsible for drug metabolism, blood homeostasis, cholesterol biosynthesis, and steriodogenesis. CYP1A1, the first P450 isoform to be named, is responsible for the metabolism and biotransformation of polycyclic aromatic hydrocarbons (PAH). 3-methylcholanthrene, an extremely hazardous PAH, has been shown to induce the CYP1A1 gene through the aryl hydrocarbon receptor (AhR) pathway. Past investigations have shown that the sphingolipid, C2-ceramide, induces CYP1A1 expression when HepG2 cells are exposed to 3-methylcholanthrene. Ceramide, the hydrophobic moiety of all complex sphingolipids, is known to act as a second messenger in the cell. Unlike ceramide, dihydroceramide, the precursor of an essential molecule needed for the formation of ceramide through the de novo pathway, has been reported to be biologically inactive. It is hypothesized that structurally different sphingolipids (ceramide and dihydroceramide) modulate the ability of MC to induce CYP1A1 expression by increasing the influx of MC into the cell. To test this hypothesis, CYP1A1 enzyme activity and protein amounts were assessed by the ethoxyresorufm-o-deethylase assay and Western Blot analysis, respectively. Through confocal microscopy it was found that the increased influx of MC was correlated to the increased expression of CYP1A1 in the presence of the sphingolipids when compared to MC treated cells alone. In addition to increased influx, it was found that ceramide and dihydroceramide also caused MC to quickly localize around the nucleus of the cells. An increased influx of MC in cells and localization to the nucleus can lead to the increased expression of CYP1A1 for the biotransformation ofPAHs. This dual effect can potentially enhance the chemical carcinogenesis process through increased production of the carcinogenic metobolites of these PAHs. Sphingolipid stimulation of CYP1A1 enzyme during the biotransformation of a PAH could then enhance the incidence of chemical carcinogenesis.
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To, Wing Shu. "Effect of cellular redox and energy states on benzo[a]pyrene induced modes of death in the hepa and the HepG2 cell lines". HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1173.

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Książki na temat "HepG2 cells"

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Villeneuve, David J. A comparison of oxidative enzymes in K562 and HepG2 cells. Sudbury, Ont: Laurentian University, 1992.

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White, Angela T. Characterisation of altered gene expression in response to Oxidative stree in HepG2 cells. Birmingham: University of Birmingham, 2003.

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Andreou, Efrosini Roseann. Analysis of CYP7A1 gene regulation in HepG2 cells by reverse-transcriptase polymerase chain reaction. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Musonda, Alam Clement. Quercetin as a modulator of xenobiotic metabolism and reactive oxygen species (ROS) in human hepG2 cells. Birmingham: University of Birmingham, 1998.

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Lekas, Poli. Analysis of human CYP2E1 mRNA in a HepG2 cell line by reverse transcription-polymerase chain reaction (RT-PCR). Ottawa: National Library of Canada, 1998.

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Traynor, Russell Mark. Growth of metabolically active HepG2, human hepatoma, cells in high density cultures. 1996.

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Rajesan, Ratheishan. Effects of human milk and formula on the transcriptional regulation of cytochrome P450 3A4 in HepG2 cells. 2004.

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Części książek na temat "HepG2 cells"

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Boucher, Philippe, i Hans Gerhard Vogel. "Internalization of Labeled LDL into HepG2 Cells". W Drug Discovery and Evaluation: Pharmacological Assays, 2291–93. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-05392-9_52.

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Boucher, Philippe, i Hans Gerhard Vogel. "Internalization of Labeled LDL into HepG2 Cells". W Drug Discovery and Evaluation: Pharmacological Assays, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27728-3_52-1.

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Kelly, Lynne A. "Phytoestrogens Activate the Estrogen Receptor in HepG2 Cells". W Methods in Molecular Biology, 445–55. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3127-9_35.

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Kumagai, T., K. Takemura, S. Terada, A. Ogawa, M. Miki, M. Sasaki i H. Yamada. "Effect of Silk Protein Sericin on Hepatoblastoma HepG2 Cells". W Animal Cell Technology: Basic & Applied Aspects, 281–85. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0726-8_49.

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Donato, María Teresa, Laia Tolosa i María José Gómez-Lechón. "Culture and Functional Characterization of Human Hepatoma HepG2 Cells". W Methods in Molecular Biology, 77–93. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2074-7_5.

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Saquib, Quaiser, Maqsood A. Siddiqui, Javed Ahmad, Sabiha M. Ansari, Mohammad Faisal, Rizwan Wahab, Abdulrahman A. Alatar, Abdulaziz A. Al-Khedhairy i Javed Musarrat. "Nickel Oxide Nanoparticles Induced Transcriptomic Alterations in HEPG2 Cells". W Advances in Experimental Medicine and Biology, 163–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-72041-8_10.

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Kurowska, Elzbieta M., i John A. Manthey. "Regulation of Lipoprotein Metabolism in HepG2 Cells by Citrus Flavonoids". W Flavonoids in Cell Function, 173–79. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-5235-9_16.

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Omasa, Takeshi, i Shin Enosawa. "Construction of Liver Model with Genetically Engineered Human HepG2 Cells". W Animal Cell Technology: Basic & Applied Aspects, 25–29. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0726-8_5.

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Wu, Defeng, i Arthur I. Cederbaum. "Development and Properties of HepG2 Cells That Constitutively Express CYP2E1". W Alcohol, 137–50. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-242-7_11.

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Kurowska, Elzbieta M., Carina Banh, Shin Hasegawa i Gary D. Manners. "Regulation of Apo B Production in HepG2 Cells by Citrus Limonoids". W ACS Symposium Series, 175–84. Washington, DC: American Chemical Society, 2000. http://dx.doi.org/10.1021/bk-2000-0758.ch013.

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Streszczenia konferencji na temat "HepG2 cells"

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Шунькина, Дарья Александровна, Анастасия Ярославовна Дахневич, Ольга Геннадьевна Хазиахматова, Егор Олегович Шунькин i Валерия Владимировна Шуплецова. "STUDY OF CELL MODELS OF HEPG2 STEATOSIS AND STEATOHEPATITIS VIABILITY". W Современные научные подходы в фундаментальных и прикладных исследованиях: сборник статей международной научной конференции (Санкт­Петербург, Декабрь 2022). Crossref, 2023. http://dx.doi.org/10.37539/221216.2022.12.14.006.

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Стеатоз печени диагностируется при наличии жировых включений более 5% от массы органа. Жировая инфильтрация печени с наличием в ней очагов воспаления выделено в отдельное заболевание - стеатогепатит. Целью исследования явилась оценка жизнеспособности клеточных моделей стеатоза и стеатогепатита линии HepG2 с использованием трет-бутилгидропероксида (tBHP) и олеиновой кислоты in vitro. Добавление олеиновой кислоты приводило к снижению процента живых клеток, увеличению содержания мертвых клеток и росту площади жировых включений в клеточной линии HepG2. Liver steatosis is diagnosed in the presence of fatty inclusions of more than 5% of the organ mass. Fatty infiltration of the liver with the presence of foci of inflammation in it is singled out as a separate disease - steatohepatitis. The aim of the study was to assess the viability of cell models of steatosis and steatohepatitis of the HepG2 line using tert-butyl hydroperoxide (tBHP) and oleic acid in vitro. The addition of oleic acid led to a decrease in the percentage of living cells, an increase in the content of dead cells, and an increase in the area of fatty inclusions in the HepG2 cell line.
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Fakhar-e-Alam, M., Syed M. Usman Ali, S. Ali, S. Firdous, M. Atif, Z. H. Ibupoto, M. Willander, M. Kashif i U. Hashim. "Photodynamic damage in liver carcinoma HepG2 cells". W 2012 International Conference on Biomedical Engineering (ICoBE). IEEE, 2012. http://dx.doi.org/10.1109/icobe.2012.6179012.

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Gao, Shiyong, Yubin Ji, Chenfeng Ji i Xiang Zou. "Induction of Apoptosis in HepG2 Cells by Solanine". W 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5162948.

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Niemietz, C., S. Guttmann, V. Sandfort i H. Schmidt. "SERPINA1 levels dictate TTR expression in HepG2 cells". W 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677092.

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Vonarx-Coinsmann, Veronique, Marie-Therese Foultier, Leonor X. de Brito, Laurent Morlet i Thierry Patrice. "HepG2 human hepatocarcinomas cells sensitization by endogenous porphyrins". W Fifth International Photodynamic Association Biennial Meeting, redaktor Denis A. Cortese. SPIE, 1994. http://dx.doi.org/10.1117/12.203358.

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Meng, Xiang-Ping, Zhen Zhang, Tong-sheng Chen, Yi-fei Wang i Zhi-ping Wang. "Anti-hepatocarcinoma effects of resveratrol nanoethosomes against human HepG2 cells". W SPIE BiOS, redaktor Wei R. Chen. SPIE, 2017. http://dx.doi.org/10.1117/12.2251110.

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Gao, Jia-min, Zhi-Ping Wang, Xiang-Ping Meng, Tong-Sheng Chen i Yi-Fei Wang. "Anti-hepatocarcinoma effects of puerarin-nanoethosomes against human HepG2 cells". W Nanophotonics and Micro/Nano Optics IV, redaktorzy Zhiping Zhou i Kazumi Wada. SPIE, 2018. http://dx.doi.org/10.1117/12.2500149.

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ma, zili, Siu Kai Kong i Kam Tai Chan. "Whole-cell ROS rise in HepG2 cells induced by localized fs laser irradiation". W Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/acp.2012.ath2e.2.

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Ma, Zi Li, Siu Kai Kong i Kam Tai Chan. "Whole-cell ROS rise in HepG2 cells induced by localized fs laser irradiation". W Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/acpc.2012.ath2e.2.

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Bajaj, M. S., S. V. Rana, R. B. Wysolmerski i S. P. Bajaj. "INHIBITOR OF THE FACTOR VIIA-TISSUE FACTOR COMPLEX IS REDUCED IN PATIENTS WITH DISSEMINATED INTRAVASCULAR COAGULATION BUT NOT IN PATIENTS WITH SEVERE HEPATOCELLULAR DISEASE". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643916.

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Recently, inhibition of factor VIIa-tissue factor activity by a plasma component(s) which requires factor Xa has been described. In this communication, we have developed a specific radiometric assay (which utilizes 3H-factor IX and is sensitive to <1% of plasma level) for this inhibitor and have measured its activity in various disease states. Strikingly, the levels of this inhibitor were found to be normal in patients with advanced chronic hepatocellular disease but low in patients with disseminated intravascular coagulation (DIC). When endotoxin was used to induce DIC in rabbits, the levels of this inhibitor fell by 30 to 90%. Human umbilical vein endothelial cells (HUVE), bovine pulmonary artery endothelial cells, and a human hepatoma cell line (HepG2) all synthesized and secreted this inhibitor whereas a promyelocytic cell line (HL-60) did not and a monocytic cell line (U937) appears to synthesize only small amounts. When ammonium sulfate fractionated human plasma, and serum-free conditioned media from both HUVE and HepG2 cells were electrophoresed on sodium dodecyl sulfate acrylamide gels, two activity peaks corresponding to Mr ≃45,000 and Mr =33,000 were eluted in each case. These observations suggest that (a) the inhibitor is consumed in DIC and that (b) endothelial cells (or other cells) synthesize sufficient amounts of this inhibitor in vivo to compensate for any decreased production by liver cells. Furthermore, the inhibitor levels were found to be normal in patients on chronic warfarin therapy suggesting that the inhibitor is not a vitamin K-dependent protein.
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Raporty organizacyjne na temat "HepG2 cells"

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Li, Jing. Effects of artemisinin on proliferation and apoptosis of human liver cancer HepG2 cells: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2020. http://dx.doi.org/10.37766/inplasy2020.4.0075.

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