Academic literature on the topic 'N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP)'
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Journal articles on the topic "N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP)"
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Wang, Dahai, Oscar A. Carretero, Xiao-Yi Yang, Nour-Eddine Rhaleb, Yun-He Liu, Tang-Dong Liao, and Xiao-Ping Yang. "N-acetyl-seryl-aspartyl-lysyl-proline stimulates angiogenesis in vitro and in vivo." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 5 (November 2004): H2099—H2105. http://dx.doi.org/10.1152/ajpheart.00592.2004.
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N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a natural inhibitor of pluripotent hematopoietic stem cell proliferation, has been suggested as capable of promoting an angiogenic response. We studied whether Ac-SDKP stimulates endothelial cell proliferation, migration, and tube formation; enhances angiogenic response in the rat cornea after implantation of a tumor spheroid; and increases capillary density in rat hearts with myocardial infarction (MI). In vitro, an immortal BALB/c mouse aortic endothelial 22106 cell line was used to determine the effects of Ac-SDKP on endothelial cell proliferation and migration and tube formation. In vivo, a 9L-gliosarcoma cell spheroid (250–300 μm in diameter) was implanted in the rat cornea and vehicle or Ac-SDKP (800 μg·kg−1·day−1ip) infused via osmotic minipump. Myocardial capillary density was studied in rats with MI given either vehicle or Ac-SDKP. We found that Ac-SDKP 1) stimulated endothelial cell proliferation and migration and tube formation in a dose-dependent manner, 2) enhanced corneal neovascularization, and 3) increased myocardial capillary density. Endothelial cell proliferation and angiogenesis stimulated by Ac-SDKP could be beneficial in cardiovascular diseases such as hypertension and MI. Furthermore, because Ac-SDKP is mainly cleaved by ACE, it may partially mediate the cardioprotective effect of ACE inhibitors.
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Nakagawa, Pablo, Yunhe Liu, Tang-Dong Liao, Xiaojuan Chen, Germán E. González, Kevin R. Bobbitt, Derek Smolarek, et al. "Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 9 (November 1, 2012): H1114—H1127. http://dx.doi.org/10.1152/ajpheart.00300.2011.
Full textAbstract:
Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs.
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Castoldi, Giovanna, Cira R. T. Di Gioia, Camila Bombardi, Carla Perego, Lucia Perego, Massimiliano Mancini, Martina Leopizzi, et al. "Prevention of myocardial fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats." Clinical Science 118, no. 3 (February 1, 2010): 211–20. http://dx.doi.org/10.1042/cs20090234.
Full textAbstract:
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is a physiological tetrapeptide hydrolysed by ACE (angiotensin-converting enzyme). In experimental models of hypertension, Ac-SDKP has antifibrotic effects in the heart; however, the role of Ac-SDKP in diabetic cardiomyopathy is currently unknown. The aim of the present study was to evaluate the effect of Ac-SDKP on cardiac systolic and diastolic function, and interstitial and perivascular fibrosis in the heart of diabetic rats. Diabetes was induced in 55 Sprague–Dawley rats by streptozotocin injection. Control rats (n=18) underwent only buffer injection. Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg·kg−1 of body weight·day−1). At 2 months after the onset of diabetes, Ac-SDKP (1 mg·kg−1 of body weight·day−1) was administered by osmotic minipumps for 8 weeks to eight control rats, 13 diabetic rats, seven diabetic rats treated with ramipril and nine insulin-treated diabetic rats. Diabetic rats had a significant increase in blood glucose levels. Left ventricular interstitial and perivascular fibrosis, and TGF-β1 (transforming growth factor-β1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. Ac-SDKP administration significantly reduced left ventricular interstitial and perivascular fibrosis in diabetic rats and in diabetic rats treated with ramipril. This was accompanied by a significant reduction in active TGF-β1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. Echocardiography showed that diabetes was associated with increased end-systolic diameters, and depressed global systolic function and diastolic dysfunction, as assessed by transmitral Doppler velocity profile. These changes were completely reversed by insulin or ramipril treatment. Ac-SDKP treatment partially restored diastolic function in diabetic rats. In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-β1 and phospho-Smad2/3 levels, and improves diastolic function. Taken together, these findings suggest that, by inhibiting the TGF-β/Smad pathway, Ac-SDKP protects against the development of diabetic cardiomyopathy.
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Lin, Chun-Xia, Nour-Eddine Rhaleb, Xiao-Ping Yang, Tang-Dong Liao, Martin A. D'Ambrosio, and Oscar A. Carretero. "Prevention of aortic fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in angiotensin II-induced hypertension." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H1253—H1261. http://dx.doi.org/10.1152/ajpheart.00481.2008.
Full textAbstract:
Fibrosis is an important component of large conduit artery disease in hypertension. The endogenous tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory and antifibrotic effects in the heart and kidney. However, it is not known whether Ac-SDKP has an anti-inflammatory and antifibrotic effect on conduit arteries such as the aorta. We hypothesize that in ANG II-induced hypertension Ac-SDKP prevents aortic fibrosis and that this effect is associated with decreased protein kinase C (PKC) activation, leading to reduced oxidative stress and inflammation and a decrease in the profibrotic cytokine transforming growth factor-β1 (TGF-β1) and phosphorylation of its second messenger Smad2. To test this hypothesis we used rats with ANG II-induced hypertension and treated them with either vehicle or Ac-SDKP. In this hypertensive model we found an increased collagen deposition and collagen type I and III mRNA expression in the aorta. These changes were associated with increased PKC activation, oxidative stress, intercellular adhesion molecule (ICAM)-1 mRNA expression, and macrophage infiltration. TGF-β1 expression and Smad2 phosphorylation also increased. Ac-SDKP prevented these effects without decreasing blood pressure or aortic hypertrophy. Ac-SDKP also enhanced expression of inhibitory Smad7. These data indicate that in ANG II-induced hypertension Ac-SDKP has an aortic antifibrotic effect. This effect may be due in part to inhibition of PKC activation, which in turn could reduce oxidative stress, ICAM-1 expression, and macrophage infiltration. Part of the effect of Ac-SDKP could also be due to reduced expression of the profibrotic cytokine TGF-β1 and inhibition of Smad2 phosphorylation.
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Liao, Tang-Dong, Pablo Nakagawa, Branislava Janic, Martin D'Ambrosio, Morel E. Worou, Edward L. Peterson, Nour-Eddine Rhaleb, Xiao-Ping Yang, and Oscar A. Carretero. "N-Acetyl-Seryl-Aspartyl-Lysyl-Proline: mechanisms of renal protection in mouse model of systemic lupus erythematosus." American Journal of Physiology-Renal Physiology 308, no. 10 (May 15, 2015): F1146—F1154. http://dx.doi.org/10.1152/ajprenal.00039.2015.
Full textAbstract:
Systemic lupus erythematosus is an autoimmune disease characterized by the development of auto antibodies against a variety of self-antigens and deposition of immune complexes that lead to inflammation, fibrosis, and end-organ damage. Up to 60% of lupus patients develop nephritis and renal dysfunction leading to kidney failure. N-acetyl-seryl-aspartyl-lysyl-proline, i.e., Ac-SDKP, is a natural tetrapeptide that in hypertension prevents inflammation and fibrosis in heart, kidney, and vasculature. In experimental autoimmune myocarditis, Ac-SDKP prevents cardiac dysfunction by decreasing innate and adaptive immunity. It has also been reported that Ac-SDKP ameliorates lupus nephritis in mice. We hypothesize that Ac-SDKP prevents lupus nephritis in mice by decreasing complement C5-9, proinflammatory cytokines, and immune cell infiltration. Lupus mice treated with Ac-SDKP for 20 wk had significantly lower renal levels of macrophage and T cell infiltration and proinflammatory chemokine/cytokines. In addition, our data demonstrate for the first time that in lupus mouse Ac-SDKP prevented the increase in complement C5-9, RANTES, MCP-5, and ICAM-1 kidney expression and it prevented the decline of glomerular filtration rate. Ac-SDKP-treated lupus mice had a significant improvement in renal function and lower levels of glomerular damage. Ac-SDKP had no effect on the production of autoantibodies. The protective Ac-SDKP effect is most likely achieved by targeting the expression of proinflammatory chemokines/cytokines, ICAM-1, and immune cell infiltration in the kidney, either directly or via C5-9 proinflammatory arm of complement system.
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Romero, Cesar A., Nitin Kumar, Pablo Nakagawa, Morel E. Worou, Tang-Dong Liao, Edward L. Peterson, and Oscar A. Carretero. "Renal release of N-acetyl-seryl-aspartyl-lysyl-proline is part of an antifibrotic peptidergic system in the kidney." American Journal of Physiology-Renal Physiology 316, no. 1 (January 1, 2019): F195—F203. http://dx.doi.org/10.1152/ajprenal.00270.2018.
Full textAbstract:
The antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is released from thymosin-β4 (Tβ4) by the meprin-α and prolyl oligopeptidase (POP) enzymes and is hydrolyzed by angiotensin-converting enzyme (ACE). Ac-SDKP is present in urine; however, it is not clear whether de novo tubular release occurs or if glomerular filtration is the main source. We hypothesized that Ac-SDKP is released into the lumen of the nephrons and that it exerts an antifibrotic effect. We determined the presence of Tβ4, meprin-α, and POP in the kidneys of Sprague-Dawley rats. The stop-flow technique was used to evaluate Ac-SDKP formation in different nephron segments. Finally, we decreased Ac-SDKP formation by inhibiting the POP enzyme and evaluated the long-term effect in renal fibrosis. The Tβ4 precursor and the releasing enzymes meprin-α and POP were expressed in the kidneys. POP enzyme activity was almost double that in the renal medulla compared with the renal cortex. With the use of the stop-flow technique, we detected the highest Ac-SDKP concentrations in the distal nephron. The infusion of a POP inhibitor into the kidney decreased the amount of Ac-SDKP in distal nephron segments and in the proximal nephron to a minor extent. An ACE inhibitor increased the Ac-SDKP content in all nephron segments, but the increase was highest in the distal portion. The chronic infusion of a POP inhibitor increased kidney medullary fibrosis, which was prevented by Ac-SDKP. We conclude that Ac-SDKP is released by the nephron and is part of an important antifibrotic system in the kidney.
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Peng, Hongmei, Jiang Xu, Xiao-Ping Yang, Kamal M. Kassem, Imane A. Rhaleb, Ed Peterson, and Nour-Eddine Rhaleb. "N-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice." Canadian Journal of Physiology and Pharmacology 97, no. 8 (August 2019): 753–65. http://dx.doi.org/10.1139/cjpp-2019-0047.
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Myocardial infarction (MI) in mice results in cardiac rupture at 4–7 days after MI, whereas cardiac fibrosis and dysfunction occur later. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic, and pro-angiogenic properties. We hypothesized that Ac-SDKP reduces cardiac rupture and adverse cardiac remodeling, and improves function by promoting angiogenesis and inhibiting detrimental reactive fibrosis and inflammation after MI. C57BL/6J mice were subjected to MI and treated with Ac-SDKP (1.6 mg/kg per day) for 1 or 5 weeks. We analyzed (1) intercellular adhesion molecule-1 (ICAM-1) expression; (2) inflammatory cell infiltration and angiogenesis; (3) gelatinolytic activity; (4) incidence of cardiac rupture; (5) p53, the endoplasmic reticulum stress marker CCAAT/enhancer binding protein homology protein (CHOP), and cardiomyocyte apoptosis; (6) sarcoplasmic reticulum Ca2+ ATPase (SERCA2) expression; (7) interstitial collagen fraction and capillary density; and (8) cardiac remodeling and function. Acutely, Ac-SDKP reduced cardiac rupture, decreased ICAM-1 expression and the number of infiltrating macrophages, decreased gelatinolytic activity, p53 expression, and myocyte apoptosis, but increased capillary density in the infarction border. Chronically, Ac-SDKP improved cardiac structures and function, reduced CHOP expression and interstitial collagen fraction, and preserved myocardium SERCA2 expression. Thus, Ac-SDKP decreased cardiac rupture, ameliorated adverse cardiac remodeling, and improved cardiac function after MI, likely through preserved SERCA2 expression and inhibition of endoplasmic reticulum stress.
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González, Germán E., Nour-Eddine Rhaleb, Pablo Nakagawa, Tang-Dong Liao, Yunhe Liu, Pablo Leung, Xiangguo Dai, Xiao-Ping Yang, and Oscar A. Carretero. "N-acetyl-seryl-aspartyl-lysyl-proline reduces cardiac collagen cross-linking and inflammation in angiotensin II-induced hypertensive rats." Clinical Science 126, no. 1 (September 9, 2013): 85–94. http://dx.doi.org/10.1042/cs20120619.
Full textAbstract:
We have reported previously that Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) reduces fibrosis and inflammation (in macrophages and mast cells). However, it is not known whether Ac-SDKP decreases collagen cross-linking and lymphocyte infiltration; lymphocytes modulate both collagen cross-linking and ECM (extracellular matrix) formation in hypertension. Thus we hypothesized that (i) in AngII (angiotensin II)-induced hypertension, Ac-SDKP prevents increases in cross-linked and total collagen by down-regulating LOX (lysyl oxidase), the enzyme responsible for cross-linking, and (ii) these effects are associated with decreased pro-fibrotic cytokine TGFβ (transforming growth factor β) and the pro-inflammatory transcription factor NF-κB (nuclear factor κB) and CD4+/CD8+ lymphocyte infiltration. We induced hypertension in rats by infusing AngII either alone or combined with Ac-SDKP for 3 weeks. Whereas Ac-SDKP failed to lower BP (blood pressure) or LV (left ventricular) hypertrophy, it did prevent AngII-induced increases in (i) cross-linked and total collagen, (ii) LOX mRNA expression and LOXL1 (LOX-like 1) protein, (iii) TGFβ expression, (iv) nuclear translocation of NF-κB, (v) CD4+/CD8+ lymphocyte infiltration, and (vi) CD68+ macrophages infiltration. In addition, we found a positive correlation between CD4+ infiltration and LOXL1 expression. In conclusion, the effect of Ac-SDKP on collagen cross-linking and total collagen may be due to reduced TGFβ1, LOXL1, and lymphocyte and macrophage infiltration, and its effect on inflammation could be due to lower NF-κB.
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Chan, Gary C. W., Wai Han Yiu, Hao Jia Wu, Dickson W. L. Wong, Miao Lin, Xiao Ru Huang, Hui Yao Lan, and Sydney C. W. Tang. "N-Acetyl-seryl-aspartyl-lysyl-proline Alleviates Renal Fibrosis Induced by Unilateral Ureteric Obstruction in BALB/C Mice." Mediators of Inflammation 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/283123.
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To expand the armamentarium of treatment for chronic kidney disease (CKD), we explored the utility of boosting endogenously synthesized N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is augmented by inhibition of the angiotensin converting enzyme. Male BALB/c mice underwent unilateral ureteral ligation (UUO) or sham operation and received exogenously administered Ac-SDKP delivered via a subcutaneous osmotic minipump or Captopril treatment by oral gavage. Seven days after UUO, there were significant reductions in the expression of both collagen 1 and collagen 3 in kidneys treated with Ac-SDKP or Captopril, and there was a trend towards reductions in collagen IV,α-SMA, and MCP-1 versus control. However, no significant attenuation of interstitial injury or macrophage infiltration was observed. These findings are in contrary to observations in other models and underscore the fact that a longer treatment time frame may be required to yield anti-inflammatory effects in BALB/c mice treated with Ac-SDKP compared to untreated mice. Finding an effective treatment regimen for CKD requires fine-tuning of pharmacologic protocols.
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Liu, Yun-He, Martin D'Ambrosio, Tang-dong Liao, Hongmei Peng, Nour-Eddine Rhaleb, Umesh Sharma, Sabine André, Hans-J. Gabius, and Oscar A. Carretero. "N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 2 (February 2009): H404—H412. http://dx.doi.org/10.1152/ajpheart.00747.2008.
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Galectin-3 (Gal-3) is secreted by activated macrophages. In hypertension, Gal-3 is a marker for hypertrophic hearts prone to develop heart failure. Gal-3 infused in pericardial sac leads to cardiac inflammation, remodeling, and dysfunction. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a naturally occurring tetrapeptide, prevents and reverses inflammation and collagen deposition in the heart in hypertension and heart failure postmyocardial infarction. In the present study, we hypothesize that Ac-SDKP prevents Gal-3-induced cardiac inflammation, remodeling, and dysfunction, and these effects are mediated by the transforming growth factor (TGF)-β/Smad3 signaling pathway. Adult male rats were divided into four groups and received the following intrapericardial infusion for 4 wk: 1) vehicle (saline, n = 8); 2) Ac-SDKP (800 μg·kg−1·day−1, n = 8); 3) Gal-3 (12 μg/day, n = 7); and 4) Ac-SDKP + Gal-3 ( n = 7). Left ventricular ejection fraction, cardiac output, and transmitral velocity were measured by echocardiography; inflammatory cell infiltration, cardiomyocyte hypertrophy, and collagen deposition in the heart by histological and immunohistochemical staining; and TGF-β expression and Smad3 phosphorylation by Western blot. We found that, in the left ventricle, Gal-3 1) enhanced macrophage and mast cell infiltration, increased cardiac interstitial and perivascular fibrosis, and causes cardiac hypertrophy; 2) increased TGF-β expression and Smad3 phosphorylation; and 3) decreased negative change in pressure over time response to isoproterenol challenge, ratio of early left ventricular filling phase to atrial contraction phase, and left ventricular ejection fraction. Ac-SDKP partially or completely prevented these effects. We conclude that Ac-SDKP prevents Gal-3-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction, possibly via inhibition of the TGF-β/Smad3 signaling pathway.
Dissertations / Theses on the topic "N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP)"
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CORRADI, BARBARA. "Ruolo di N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) nella progressione della Nefropatia Diabetica." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43715.
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La nefropatia diabetica è la principale causa di insufficienza renale terminale. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP), tetrapeptide fisiologicamente presente nel plasma e nei tessuti, viene idrolizzato dall’ enzima di conversione dell’angiotensina. Il tetrapeptide ha un effetto antifibrotico sul sistema cardiovascolare e nel rene in modelli sperimentali di ipertensione, infarto del miocardio e nefropatie. Lo scopo del nostro lavoro è stato studiare gli effetti antifibrotici di Ac-SDKP in un modello sperimentale di nefropatia diabetica, e il potenziale effetto additivo del tetrapeptide, in aggiunta al singolo trattamento con ACE-inibitore, sulla progressione della fibrosi renale.
A 28 ratti Sprague Dawley e’ stato indotto diabete con un’iniezione di streptozotocina, mentre a 10 ratti controllo e’ stata somministrata solo soluzione tampone. Dopo l’ insorgenza di diabete a 11 ratti è stato somministrato un inibitore dell’enzima di conversione dell’angiotensina (ACE-inibitore, ramipril 3 mg/Kg/die). Dopo 2 mesi di trattamento con ACE-inibitore a 7 ratti diabetici e a 6 ratti diabetici trattati con ramipril è stato somministrato per 8 settimane Ac-SDKP, alla dose di 1 mg/Kg/die, attraverso minipompe osmotiche impiantate nella regione infrascapolare. A 10 ratti controllo, a 10 ratti diabetici e a 5 ratti diabetici trattati con ramipril la minipompa osmotica rilasciava, per lo stesso periodo, solo soluzione fisiologica.
Al termine del trattamento i ratti diabetici rispetto ai ratti del gruppo di controllo mostravano un significativo aumento del livello di glucosio, dell’ escrezione urinaria di albumina, della fibrosi renale e una significativa riduzione dell’espressione di nefrina a livello dei glomeruli. La somministrazione di Ac-SDKP riduceva significativamente la fibrosi renale nei ratti diabetici, ma non modificava significativamente l’escrezione urinaria di albumina. Il trattamento farmacologico con ACE-inibitore causava una significativa diminuzione dell’albuminuria e della fibrosi renale, ripristinando l’espressione della nefrina glomerulare. La somministrazione di Ac-SDKP, in aggiunta al trattamento con ACE-inibitore, riduceva ulteriormente la fibrosi renale rispetto al solo trattamento con ramipril, mentre non incrementava l’effetto antiproteinurico dell’ACE-inibitore.
In conclusione questo studio ha dimostrato che la somministrazione di Ac-SDKP in un modello di nefropatia diabetica riduce la fibrosi renale. Il trattamento combinato (Ac-SDKP
+ ACE-inibitore) aumenta l’effetto antifibrotico dell’ACE-inibitore nel tessuto renale, suggerendo il benefico effetto di questa associazione farmacologica nel trattamento della nefropatia diabetica.