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10.2147/DDDT.S100095

http://scihub22266oqcxt.onion/10.2147/DDDT.S100095
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C4862356!4862356!27217725
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suck abstract from ncbi


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pmid27217725      Drug+Des+Devel+Ther 2016 ; 10 (ä): 1581-8
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  • Spirolactone provides protection from renal fibrosis by inhibiting the endothelial?mesenchymal transition in isoprenaline-induced heart failure in rats #MMPMID27217725
  • Zhou H; Xi D; Liu J; Zhao J; Chen S; Guo Z
  • Drug Des Devel Ther 2016[]; 10 (ä): 1581-8 PMID27217725show ga
  • Background: Fibrosis results in excessive accumulation of extracellular matrix proteins, collagen component alteration, and abnormalities in structure and is partly derived from a process called the endothelial?mesenchymal transition involving transforming growth factor ? (TGF-?). We investigated whether spironolactone, an aldosterone receptor blocker, attenuated isoprenaline (Iso)-induced heart failure in rats and also studied the mechanism for the same. Methods: Sprague?Dawley rats were subcutaneously injected with Iso to induce heart failure, which promoted renal fibrosis; rats with spironolactone treatment were given a gavage of spironolactone (30 or 60 mg/kg/d, for 21 days). Cardiac function and fibrosis indices were measured. Pathological alterations and expression of Type I and III collagen, ?-smooth muscle actin, cluster of differentiation-31, and TGF-? were examined. Results: In Iso-induced heart failure in rats, spironolactone significantly improved cardiac function and decreased myocardial fibrosis, reduced collagen fibrous proliferation in kidney, reduced expression of Type I and III collagen, increased the expression of cluster of differentiation-31, and decreased the expression of ?-smooth muscle actin and TGF-?. Conclusion: Spironolactone may prevent renal fibrosis by inhibiting the endothelial?mesenchymal transition.
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