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

B. Liu, N. Jia, H.-L. Wei, M. Lan, J.-M. Liu, Y.-Z. Xue

Department of Cardiology, Beijing Hospital, National Center of Gerontology, Beijing, China. xyz930911@163.com

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• Cardiology

OBJECTIVE: 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.

MATERIALS AND METHODS: 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.

RESULTS: 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.

CONCLUSIONS: Knockdown of p66ShcA can activate Keap1/Nrf2 pathway, which inhibits H2O2-induced oxidative stress and inflammation in H9c2 cells.

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