Fig. 7

Summary diagram of the proposed mechanisms underlying protective effects of C3G against glutamate-induced oxidative/ER stress apoptosis in HT22 cells. Prolonged glutamate-induced ROS production stimulates oxidative stress lead to ER stress. The resultant oxidative stress activate the specific ER stress apoptosis mechanisms involving calcium ion-mediated calpain activation contribute to caspase-12 cascades apoptosis signal, together with CHOP apoptosis pathway. C3G is able to reduce ROS and trigger survival marker proteins including p-ERK/ERK and Nrf2 expression, leading to an increase level of the endogenous antioxidant and phase II detoxifying enzymes function. As a consequence, these effects resulted in the inhibition of apoptotic-ER stress signaling proteins and enhancing HT22 neuronal cell survival via the ERK/Nrf2 signaling pathway