scholarly journals Retraction of: Roles of the Exogenous H2S-Mediated SR-A Signaling Pathway in Renal Ischemia/Reperfusion Injury in Regulating Endoplasmic Reticulum Stress-Induced Autophagy in a Rat Model

2021 ◽  
Vol 55 (5) ◽  
pp. 663-663
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Hydroxysafflor Yellow A Attenuates Renal Ischemia- Reperfusion Injury in a Rat Model

2012 ◽  
Vol 9 (10) ◽  
pp. 967-972
Author(s):  
Weiran Chai ◽  
Wenhui Zhang ◽  
Zhu Jin ◽  
Yanqian Zheng ◽  
Peiyao Jin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Hydroxysafflor Yellow A ◽  
Renal Ischemia Reperfusion Injury

scholarly journals Remote ischemic per-conditioning protects against renal ischemia–reperfusion injury via suppressing gene expression of TLR4 and TNF-α in rat model

2019 ◽  
Vol 97 (2) ◽  
pp. 112-119 ◽  
Author(s):  
Firouzeh Gholampour ◽  
Jamshid Roozbeh ◽  
Sahar Janfeshan ◽  
Zeinab Karimi
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Antioxidant Systems ◽  
Tlr4 Signaling ◽  
Tnf Α ◽  
Renal Ischemia Reperfusion Injury ◽  
Tlr4 Signaling Pathway

The pathogenesis of renal ischemia–reperfusion injury (IRI) involves both inflammatory processes and oxidative stress in the kidney. This study determined whether remote ischemic per-conditioning (RIPerC) is mediated by toll-like receptor 4 (TLR4) signaling pathway in rats. Renal IR injury was induced by occluding renal arteries for 45 min followed by 24 h of reperfusion. RIPerC included 4 cycles of 2 min of ischemia of the left femoral artery followed by 3 min of reperfusion performed at the start of renal ischemia. Rats were divided into sham, IR, and RIPerC groups. At the end of the reperfusion period, urine, blood and tissue samples were gathered. IR created kidney dysfunction, as ascertained by a significant decrease in creatinine clearance and a significant increase in sodium fractional excretion. These changes occurred in concert with a decrease in the activities of glutathione peroxidase, catalase, and superoxide dismutase with an increment in malondialdehyde levels, mRNA expression levels of TLR4 and tumor necrosis factor α (TNF-α), and histological damage in renal tissues. RIPerC treatment diminished all these changes. This study demonstrates that RIPerC has protective effects on the kidney after renal IR, which might be related to the inhibition of the TLR4 signaling pathway and augmentation of antioxidant systems.

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