| 000 | 03314cam a2200349 a 4500 | ||
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| 003 | EG-GiCUC | ||
| 005 | 20250223032211.0 | ||
| 008 | 190219s2018 ua dh f m 000 0 eng d | ||
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_aEG-GiCUC _beng _cEG-GiCUC |
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| 041 | 0 | _aeng | |
| 049 | _aDeposite | ||
| 097 | _aM.Sc | ||
| 099 | _aCai01.08.09.M.Sc.2018.Na.S | ||
| 100 | 0 | _aNada Muhammad Kamel Muhammad | |
| 245 | 1 | 0 |
_aStudy on the effect of saxagliptin on renal injury induced by ischemia/reperfusion in rats / _cNada Muhammad Kamel Muhammad ; Supervised Dalaal M. Abdallah , Hanan S. Elabhar , May Ahmad Galal |
| 246 | 1 | 5 | _aدراسة تأثير الساكساجليبتين فى الإعتلال الكلوى المحدث عن طريق إعاقة تدفق الدم إلى الكلى ثم إعادة التروية فى الجرذان |
| 260 |
_aCairo : _bNada Muhammad Kamel Muhammad , _c2018 |
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| 300 |
_a118 P. : _bcharts , facsimiles ; _c25cm |
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| 502 | _aThesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology | ||
| 520 | _aSaxagliptin, 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 | ||
| 530 | _aIssued also as CD | ||
| 653 | 4 | _aGLP-1 | |
| 653 | 4 | _aKim-1 | |
| 653 | 4 | _aSaxagliptin | |
| 700 | 0 |
_aDalaal Moustafa Abdallah , _eSupervisor |
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| 700 | 0 |
_aHanan Salah Eldin Hamdy Elabhar , _eSupervisor |
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| 700 | 0 |
_aMay Ahmad Galal , _eSupervisor |
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| 856 | _uhttp://172.23.153.220/th.pdf | ||
| 905 |
_aNazla _eRevisor |
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| 905 |
_aSamia _eCataloger |
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| 942 |
_2ddc _cTH |
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| 999 |
_c70344 _d70344 |
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