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Study on the effect of saxagliptin on renal injury induced by ischemia/reperfusion in rats / Nada Muhammad Kamel Muhammad ; Supervised Dalaal M. Abdallah , Hanan S. Elabhar , May Ahmad Galal

By: Contributor(s): Material type: TextTextLanguage: English Publication details: Cairo : Nada Muhammad Kamel Muhammad , 2018Description: 118 P. : charts , facsimiles ; 25cmOther title:
  • دراسة تأثير الساكساجليبتين فى الإعتلال الكلوى المحدث عن طريق إعاقة تدفق الدم إلى الكلى ثم إعادة التروية فى الجرذان [Added title page title]
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Dissertation note: Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology Summary: Saxagliptin, a dipeptidyl peptidase (DPP)-4 inhibitor, is currently used in type 2 diabetes mellitus; however, its potential role against the renal ischemia/reperfusion (I/R) insult has not been elucidated. Using the renal I/R model in Wistar rats, saxagliptin (10 and 30 mg/kg) operated through different axes to enhance renal perfusion, it increased the renal kidney injury molecule-1/p-STAT3 (Tyr705)/hypoxia inducible factor-1Ü/vascular endothelial growth factor (VEGF) pathway to enhance angiogenesis. Additionally, by inhibiting DPP-4, saxagliptin spared the stromal cell derived factor-1Ü and increased its receptor, the chemokine receptor (CXCR) 4, to trigger vasculogenesis by enhancing the migration of endothelial progenitor cells (EPCs), designated by the elevated immunoreactive CD133+ cells. The gliptin also saved glucagon like peptide-1, with the subsequent increase in cAMP that positively influenced VEGF and CXCR4. Another pathway stimulated by saxagliptin was the atrial natriuretic peptide/endothelial nitric oxide synthase that increased nitric oxide to provoke angiogenesis and renal vasodilation. These interrelated molecules improved kidney function of rats subjected to acute renal I/R, as evidenced by the decreased serum creatinine, blood urea nitrogen, and cystatin C, increased serum albumin, and improved the histological structure. Additionally, saxaglipitin suppressed the renal phosphor-serine 536 nuclear factor-mB p65, monocyte chemoattractant protein-1, myeloperoxidase, malondialdehyde, and tumor necrosis factor-Ü, while boosted glutathione. Accordingly, saxagliptin, dose dependently, ameliorated I/R-induced renal damage via its anti-inflammatory and antioxidant activities, besides the enhancement of neovascularization through improving tissue perfusion and homing of bone marrow derived EPCs to intercede repair processes
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Thesis Thesis قاعة الرسائل الجامعية - الدور الاول المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2018.Na.S (Browse shelf(Opens below)) Not for loan 01010110077243000
CD - Rom CD - Rom مخـــزن الرســائل الجـــامعية - البدروم المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2018.Na.S (Browse shelf(Opens below)) 77243.CD Not for loan 01020110077243000

Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

Saxagliptin, a dipeptidyl peptidase (DPP)-4 inhibitor, is currently used in type 2 diabetes mellitus; however, its potential role against the renal ischemia/reperfusion (I/R) insult has not been elucidated. Using the renal I/R model in Wistar rats, saxagliptin (10 and 30 mg/kg) operated through different axes to enhance renal perfusion, it increased the renal kidney injury molecule-1/p-STAT3 (Tyr705)/hypoxia inducible factor-1Ü/vascular endothelial growth factor (VEGF) pathway to enhance angiogenesis. Additionally, by inhibiting DPP-4, saxagliptin spared the stromal cell derived factor-1Ü and increased its receptor, the chemokine receptor (CXCR) 4, to trigger vasculogenesis by enhancing the migration of endothelial progenitor cells (EPCs), designated by the elevated immunoreactive CD133+ cells. The gliptin also saved glucagon like peptide-1, with the subsequent increase in cAMP that positively influenced VEGF and CXCR4. Another pathway stimulated by saxagliptin was the atrial natriuretic peptide/endothelial nitric oxide synthase that increased nitric oxide to provoke angiogenesis and renal vasodilation. These interrelated molecules improved kidney function of rats subjected to acute renal I/R, as evidenced by the decreased serum creatinine, blood urea nitrogen, and cystatin C, increased serum albumin, and improved the histological structure. Additionally, saxaglipitin suppressed the renal phosphor-serine 536 nuclear factor-mB p65, monocyte chemoattractant protein-1, myeloperoxidase, malondialdehyde, and tumor necrosis factor-Ü, while boosted glutathione. Accordingly, saxagliptin, dose dependently, ameliorated I/R-induced renal damage via its anti-inflammatory and antioxidant activities, besides the enhancement of neovascularization through improving tissue perfusion and homing of bone marrow derived EPCs to intercede repair processes

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