Autophagy plays a protective role in maintaining cellular homeostasis under physiological conditions and in helping cells to resist starvation under nutrient deprivation. Cells can excessively produce reactive oxygen species (ROS) under nutrient starvation, which can lead to organelle damage and protein misfolding, thus promoting cell death. However, it is not clear whether autophagy interacts with ROS during this process. In this study, we explored whether autophagy is involved in the protective effect of serum deprivation- induced cell apoptosis and excessive production of ROS in BV-2 cells with Atg5 knockdown. In addition, we examined the autophagy level in cells treated with N-acetylcysteine (NAC). We found that the cells grew slowly and aged, and the levels of ROS and autophagy increased after 24 h of serum deprivation. Autophagy defects significantly increased ROS levels and cell death. Compared with the starvation group, the NAC treatment group reduced the levels of ROS and autophagy (p<0.05), and decreased cell death. On conclusion, autophagy and low levels of ROS can promote microglia survival compared with autophagy defects or high levels of ROS under starvation conditions, Therefore, autophagy and moderate ROS are beneficial to maintain cellular homeostasis under pathological conditions.
KEY WORDS: Autophagy; Serum starvation; ROS; Microglia; IL-6; TNF-α.
GUO, J. & MA, K. Autophagy maintains the survival of microglia by modulating ros production under serum deprivation condition. Int. J. Morphol., 42(6):1567-1575, 2024.
