Abstract
Endoplasmic reticulum (ER)‐stress is known to induce neuronal cell death and is involved in neurodegenerative diseases including Alzheimer's diseases, Parkinson diseases, and cerebral ischemia. Apigenin, a bioactive flavonoid, is shown to have anti‐tumorigenic and anti‐inflammatory properties in various cell types. In the present study, we investigated the effect of apigenin on ER stress‐induced apoptosis and action mechanism involved in murine HT22 hippocampal neuronal cells. Apigenin blocked apoptotic cell death of HT22 cells induced by ER stress inducers, thapsigargin (TG) and brefeldin A (BFA). We showed that apigenin reduced the expression levels of unfolded protein response (UPR) proteins including C/EBP homologous protein (CHOP) and glucose response protein 78 (GRP78) and phosphorylations of MAP kinases in TG or BFA‐treated HT22 cells. We also showed that TG or BFA increased intracellular ROS accumulation and apigenin blocked ROS accumulation induced by TG or BFA. Moreover, we found that TG or BFA decreased the mitochondrial membrane potential (MMP) and apigenin inhibited this decrease in MMP by TG or BFA. These results suggest that apigenin inhibits ER stress‐induced apoptosis by reducing ROS accumulation, mitochondrial dysfunction, and CHOP induction in HT22 hippocampal neuronal cells.This work was supported by grants from KOSEF of Korean Government.
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