Abstract
Acori Tatarinowii Rhizome (ATR, the dried rhizome of Acorus tatarinowii Schott), a well-recognized traditional Chinese herbal medicine, is prescribed to treat neurological disorders. The essential oil is considered as the active fraction of ATR, and the neuroprotection of ATR essential oil (ATEO) is proven, including the protection against oxidative stress. However, the cellular mechanism of ATEO against oxidative stress has not been fully illustrated. In this study, to investigate the cellular mechanism of ATEO, the cytoprotective effect of ATEO against H2O2-induced injury was revealed in PC12 cells. ATEO treatment increased the viability of cells affected by H2O2-mediated injury, inhibited reactive oxygen species (ROS) accumulation, and induced the expression of several antioxidant proteins (SODs, GPx, and UCPs). The cytoprotective effect of ATEO was related to upregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) expression, which was counteracted by PGC-1α specific knockdown. Using inhibitor of protein kinase A (PKA), we found that cAMP-response element binding protein (CREB) activation was involved in ATEO-induced PGC-1α expression. Taken together, we suggest that ATEO effectively prevents H2O2-induced cell injury possibly through the activation of CREB/PGC-1α signaling in PC12 cells. The results provide a molecular insight into the effect of ATEO on cytoprotection against oxidative stress.