All-trans retinoic acid suppresses apoptosis in PC12 cells injured by oxygen and glucose deprivation via the retinoic acid receptor α signaling pathway.

Vitamin A (VA) has a number of important biological functions in human growth and development. Previous studies by our group demonstrated that the normal VA levels improved recovery of learning and memory function and decreased apoptosis in rats with hypoxic-ischemic brain damage (HIBD). However, it has not been fully elucidated how VA regulates the apoptosis of neuronal cells. To investigate the anti-apoptotic effect of VA, an in vitro oxygen glucose deprivation (OGD) model in PC12 cells was treated with four concentrations of all-trans-retinoic acid (ATRA), an active in vivo product of VA. Following in vitro OGD injury in PC12 cells, the percentage of apoptosis and the fluorescence intensity of the mitochondrial membrane potential (MMP) were increased in the cells, and the expression levels of B-cell lymphoma-associated X (Bax) were enhanced. ATRA treatment at 2-4 μmol/l for 24 h decreased the percentage of apoptosis and the MMP of the PC12 cells injured by OGD. ATRA at 4 μmol/l also reduced the expression levels of Bax and enhanced the expression of B-cell lymphoma 2. Furthermore, RNA interference with retinoic acid receptor α (RARα) reversed the observed effect in PC12 cells following ATRA treatment at 4 μmol/l alone. In conclusion, the present study suggested that treatment with ATRA at 4 μmol/l suppressed apoptosis of PC12 cells following OGD injury, potentially through regulation of the RARα signaling pathway. [ABSTRACT FROM AUTHOR]