Ginsenoside Rg1 alleviates H2O2-induced oxidative stress and apoptosis in bovine mammary epithelial cells through the NFE2L2 signaling pathway

Abstract Background During the lactation period, the dairy cows is often in a state of negative energy balance. An enhanced lipid mobilization alters the redox imbalance of bovine mammary epithelial cells (bMECs) due to the negative energy balance in the early stage of lactation. Ginsenoside Rg1 (Rg1), the main active components of ginseng, has been well-documented with possession of excellent antioxidant both in humans and non-ruminants. The primary objective of this study was to explore the therapeutic effect of Rg1 on H2O2-induced oxidative damage of bMECs and its molecular mechanism. Bovine MEC line MAC-T cells were pretreated with Rg1 (0.25, 0.5, 1 or 2 µM) for 24 h, followed by a H2O2 (500 µM) challenge for 24 h. Results Rg1 treatment decreased intracellular ROS and apoptosis induced by H2O2. These effects are related to the activation of NFE2L2 antioxidant response element (ARE) pathway and the inactivation of caspase / Bcl2 / p53 apoptosis pathway. MAC-T cells were transfected with NFE2L2 siRNA for 48 h, and then treated with Rg1 (2 µM) for another 24 h, followed by a H2O2 (500 µM) challenge for 24 h. The protective effect of Rg1 on H2O2-induced intracellular ROS accumulation and apoptosis was eliminated after transfection with NFE2L2 siRNA. Conclusions These results suggest that NFE2L2 is necessary for the protective mechanism of Rg1 on H2O2-induced oxidative damage of bMECs. Thus, Rg1 might be a potent antioxidant in vivo that could be administered to ruminant animals during stressful periods such as the transition into lactation.