https://www.selleckchem.com/products/jq1.html
The in vitro study showed that Se alleviated (P less then 0.05) AFB1-reduced cell viability and induced (P less then 0.05) ROS and ferroptosis in H9C2 cardiac cells. It also downregulated (P less then 0.05) two ferroptosis activators (long-chain acyl-CoA synthetase 4 and solute carrier family 11 Member 2) in the AFB1-treated groups in the H9C2 cells. In conclusion, this study illustrated that Se alleviates AFB1-induced cardiotoxicity and cardiomyocyte damage potentially related to the regulation of redox status, 4 selenoproteins, and ferrop
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