Knockdown of p66ShcA activates Nrf2 pathway to protect cardiomyocytes from oxidative stress and inflammation induced by H2O2.

Oxidative stress and inflammation are the most common causes of myocardial ischemia and hypoxia. This article focuses on the effect of p66ShcA on H2O2-induced cardiomyocytes. The p66ShcA knockdown model of H9c2 cells was constructed by plasmid transfection. After treatment of different groups with H2O2, oxidative stress-related factors and inflammatory factors were detected. The expressions of SOD1, SOD2, GPX1, and GPX3 in H2O2 cells were significantly decreased, IL-1β and IL-6 expression were significantly increased, while p66ShcA siRNA negative group could promote the expression of SOD1, SOD2, GPX1, and GPX3, inhibit the expression of IL-1β and IL-6 significantly, and activates the Keap1/Nrf2 pathways. Knockdown of p66ShcA can activate Keap1/Nrf2 pathway, which inhibits H2O2-induced oxidative stress and inflammation in H9c2 cells.