Protective effect of against experimental hepatic ischemia reperfusion injury downregulating oxidative stress, inflammation, and apoptosis.

Hepatic ischemia/reperfusion (Hep I/R) is a great health burden during hepatic transplantation surgery. The present work aimed to examine the mitigative effect of against Hep I/R and its underlying protective mechanisms. The animals in the present research were classified into four equal experimental groups (n=6): the sham group, sham+ group, Hep I/R group, and Hep I/R+ group. Hepatic ischemia results in liver impairment, as evidenced by elevated liver enzyme levels and altered liver histology. It also reduced antioxidant enzyme levels and increased lipid peroxidation. Additionally, the Hep I/R group displayed significant suppression of the nuclear factor erythroid 2-related factor 2 (Nrf2)/haem oxygenase-1 pathway. There was a marked elevation in the expression of inflammatory markers, including nuclear factor kappa beta (NF-κB), tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and myloperoxidase, and NOD-like receptor protein 3 (NLRP3) and caspase-1. Furthermore, the levels of apoptotic markers such as caspase-3 and Bax were greater than those in the sham groups. Pretreatment with significantly protected against Hep I/R by reversing these effects. Rats pretreated with exhibited a hepatoprotective effect against Hep I/R through its inhibition of the NF-κB and NLRP3 cascades and Nrf2 stimulation.