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10.18632/oncotarget.24733 http://scihub22266oqcxt.onion/10.18632/oncotarget.24733 C5966262!5966262!29849933     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2018 ; 9 (36): 24199-208 Nephropedia Template TP {{tp|p=29849933|t=2018. Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion |pdf=|usr=}}{{29849933}} gab.com Text Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29849933 #FOAvip Acute kidney injury (AKI) has been widely recognized as an important risk factor leading to the occurrence and progression of chronic kidney disease (CKD). Thus, development of the strategies in retarding the transition of AKI to CKD is becoming a hot research field. Recently, accumulating evidence suggested a pathogenic role of mitochondrial dysfunction in both AKI and CKD. Therefore, in the present study, we evaluated the effect of mitochondrial complex 1 inhibition by rotenone on the chronic renal damage induced by acute ischemia-reperfusion. The mice were treated with 45 min unilateral renal ischemia and reperfusion (I/R) to induce an acute renal injury. After three days of I/R injury, rotenone at a dose of 200 ppm in food was administered to the mice. Strikingly, after three weeks treatment with rotenone, we found that the unilateral I/R-induced tubular damage, tubulointerstitial fibrosis were all attenuated by rotenone as determined by the tubular injury score, Masson staining, and the levels of collagen-I, collagen-III, fibronectin, PAI-1, and TGF-?. Meanwhile, the enhanced inflammatory markers of TNF-?, IL-1?, IL-6, and IL-18 and apoptotic markers of Bax and caspase-3 were all significantly blunted by inhibiting mitochondrial complex-1. Moreover, rotenone treatment also partially protected the mitochondria as shown by the restoration of mitochondrial SOD (SOD2), ATPB, and mitochondrial DNA copy number. These findings suggested that inhibition of mitochondrial complex-1 activity by rotenone could retard the progression of AKI to CKD probably via protecting the mitochondrial function to some extent. Twit Text FOAVip Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29849933 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29849933 #FOAvip English Wikipedia <ref>{{Cite pmid|29849933}}</ref> Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion #MMPMID29849933 Zhang W; Sha Y; Wei K; Wu C; Ding D; Yang Y; Zhu C; Zhang Y; Ding G; Zhang A; Jia Z; Huang S Oncotarget 2018[May]; 9 (36): 24199-208 PMID29849933show ga Acute kidney injury (AKI) has been widely recognized as an important risk factor leading to the occurrence and progression of chronic kidney disease (CKD). Thus, development of the strategies in retarding the transition of AKI to CKD is becoming a hot research field. Recently, accumulating evidence suggested a pathogenic role of mitochondrial dysfunction in both AKI and CKD. Therefore, in the present study, we evaluated the effect of mitochondrial complex 1 inhibition by rotenone on the chronic renal damage induced by acute ischemia-reperfusion. The mice were treated with 45 min unilateral renal ischemia and reperfusion (I/R) to induce an acute renal injury. After three days of I/R injury, rotenone at a dose of 200 ppm in food was administered to the mice. Strikingly, after three weeks treatment with rotenone, we found that the unilateral I/R-induced tubular damage, tubulointerstitial fibrosis were all attenuated by rotenone as determined by the tubular injury score, Masson staining, and the levels of collagen-I, collagen-III, fibronectin, PAI-1, and TGF-?. Meanwhile, the enhanced inflammatory markers of TNF-?, IL-1?, IL-6, and IL-18 and apoptotic markers of Bax and caspase-3 were all significantly blunted by inhibiting mitochondrial complex-1. Moreover, rotenone treatment also partially protected the mitochondria as shown by the restoration of mitochondrial SOD (SOD2), ATPB, and mitochondrial DNA copy number. These findings suggested that inhibition of mitochondrial complex-1 activity by rotenone could retard the progression of AKI to CKD probably via protecting the mitochondrial function to some extent. äRotenone ameliorates chronic renal injury caused by acute ischemia/rep(epmc).pdf DeepDyve Pubget Overpricing