Xanthotoxol inhibits cerebral ischemia/reperfusion injury-induced hippocampal neuronal cell apoptosis through suppressing the p38 MAPK and JNK signaling pathways

Xanthohumol (XN) is a prenylated chalcone derived from hops (Humuluslupulus L.). Several studies showed that XN exhibited potent neuroprotective activity. However, the precise mechanism and effect of XN in cerebral ischemia/reperfusion (I/R) injury needs further investigations. In the present study, we investigated the role of XN in regulating oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuron apoptosis. The current study demonstrated that XN pretreatment ameliorates OGD/R-induced cell viability loss and decreased OGD/R-induced ROS generation and MDA level in hippocampal neurons. XN also dose-dependently inhibited the expression of Bax and caspase-3, and enhanced the expression of Bcl-2 in hippocampal neurons. At last, we found that XN pretreatment inhibits OGD/R-induced activation of p38 MAPK and JNK signaling pathways in hippocampal neurons. In conclusion, our present study showed that XN protected neuronal injury induced by OGD/R through suppression of p38 MAPK and JNK signaling pathways. This study provides evidence that XN may serve as a potential therapeutic agent for treatment of ischemic diseases.