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10.1155/2018/1072805

http://scihub22266oqcxt.onion/10.1155/2018/1072805
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C6051050!6051050!30057668
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suck abstract from ncbi


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pmid30057668      Oxid+Med+Cell+Longev 2018 ; 2018 (ä): ä
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  • Effects of Post Ischemia-Reperfusion Treatment with Trimetazidine on Renal Injury in Rats: Insights on Delayed Renal Fibrosis Progression #MMPMID30057668
  • Park JH; Jun JH; Shim JK; Shin EJ; Shin E; Kwak YL
  • Oxid Med Cell Longev 2018[]; 2018 (ä): ä PMID30057668show ga
  • Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3?mg/kg or 0.9% saline was given intraperitoneally once upon reperfusion or daily thereafter for 5?d or 8?w. Renal histologic changes and related signaling proteins were assessed. After 24?h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1?, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5?d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1?-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8?w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.
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