Collectively, rhEPO suppressed LPS-induced cell apoptosis via AMPK/SIRT1 pathway mediated autophagy, and modulating their levels may serve as potential way in preventing AKI.
SIRT1 activation and p53 deacetylation might be identified as potential targets for attenuating premature renal senescence and retarding the progression of CKD post AKI.
CONCLUSIONS NLRP3 inflammasome could act as a critical regulator promoting the process of AKI induced by LPS, and the overexpression of SIRT1 might be able to suppress the activation of NLRP3 and therefore resist the kidney injury, showing promise to be used as a target in the treatment of sepsis-induced AKI.
GA prevented LPS-induced AKI by activating SIRT1 via inhibiting the NF-κB signaling pathway, providing new insights into the function and molecular mechanism of GA in AKI.
Res increases the survival rate of septic rats by inhibiting inflammatory factors to ease AKI and promotes NF-κB-P65 de-acetylation by upregulating SIRT1.