https://www.selleckchem.com/products/4sc-202.html
6%) in the liver, to inhibit the occurrence of oxidative stress. Moreover, hepatic tissues from our experiment revealed that SCEO pre-treatment mitigated liver injury caused by oxidative stress by increasing Nrf2, HO-1, and GCL. Additionally, SCEO activated autophagy, which upregulated hepatic LC3-II and decreased p62 in APAP overdose mice ( 0.05). Our evidence demonstrated that SCEO protects hepatocytes from APAP-induced liver injury and the findings will provide a reliable theoretical basis for developing novel therapeutics. Our
Like
Comment
Share
