Oxidative stress is a risk factor for mammary health, resulting in decreased milk yield and milk quality. Application of exogenous bioactive compounds has been a research focus of antioxidation in the mammary gland. Quercetin is a flavonoid extracted from vegetables, fruits and tea which has a variety of biological activities. In this study, mouse mammary epithelial cells were treated with quercetin, and the effect and molecular mechanism of quercetin protection on hydrogen peroxide-induced oxidative stress were studied. Results showed that quercetin alleviated the cell viability, lactate dehydrogenase release, ROS accumulation and antioxidation capacity of cells challenged by hydrogen peroxide. Importantly, quercetin restored the activation of mitogen-activated protein kinase (MAPK) and nuclear factor E2-related factor 2 (Nrf2) pathways induced by hydrogen peroxide. The inhibitors of p38 MAPK and ERK affected the activation of Nrf2 pathway, suggesting that quercetin may protect mammary epithelial cells from oxidative stress by p38 MAPK-Nrf2 and ERK-Nrf2 pathways simultaneously. Moreover, the inhibitors of MAPK and Nrf2 pathways reduced the protective effects of quercetin on cell viability, the activity of CAT and the expression of GCLM. In summary, the protective effect of quercetin in mammary epithelial cells was mediated via MAPK and Nrf2 pathways.

Roles of MAPK and Nrf2 signaling pathways in quercetin alleviating redox imbalance induced by hydrogen peroxide in mammary epithelial cells

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