Hepatic Ischemia-reperfusion Injury – Inhibition of Nrf2

Inhibition of Nrf2 signaling isetin on viability, apoptosis, and oxidative stress in HR hepatocytes, suggesting that Nrf2 signaling is necessary to regulate liver IRT by fisetin. Fisetin reduces hepatic damage, cell apoptosis, and oxidative stress induced by ischemic hepatic reperfusion. In addition, fisetin played a protective role in liver IV by reducing cell apoptosis and oxidative stress in vivo and in vitro. Administration of a high concentration of fisetin promoted translocation of Nrf2 from the cytoplasm to the nucleus and increased protein expression of its downstream components, at least HO-1, in hepatic IR tissue and hepatocytes after HR. Protective effect of fisetin on hepatic ischemia-reperfusion injury by inhibiting apoptosis and oxidative stress. Results: Histopathological evaluation showed that fisetin markedly attenuated IR-induced liver injury. However, the effect of fisetin on liver IR is poorly understood. Cell apoptosis was assessed by TUNEL staining and Bax, Bcl-2, cleaved caspase-3, and cleaved PARP proteins. Oxidative stress was assessed by ROS and MDA levels as well as by SOD and GSH-Px activity. Before starting any natural, integrative or conventional treatment, it is advisable to seek the advice of a qualified health care professional. Fisetin, a type of flavonoid, is believed to protect against myocardial and brain IRT.

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