Protective effect of pig brain polypeptides against corticosterone-induced oxidative stress, inflammatory response, and apoptosis in PC12 cells.

• PBP treatment increased cell viability and decreased the release of LDH in PC12 cells incuded by CORT. • PBP reduced CORT-induced oxidative stress by decreasing ROS levels, increasing SOD, GSH-Px activities and GSH content. • PBP had inhibitory effect on the CORT-induced inflammatory response through inhibition of NF-κB signaling pathway. • PBP inhibited CORT-induced apoptosis by down-regulating mitochondrial apoptotic signaling pathway. Pig brain polypeptides (PBP), active polypeptides hydrolysate extracted from fresh porcine brain tissue, has been shown to have neuroprotective effects in both in vitro and in vivo studies. The present study aimed to explore the molecular mechanisms underlying the neuroprotective effects of PBP in corticosterone (CORT)-induced rat adrenal pheochromocytoma PC12 cells. Cell viability and lactate dehydrogenase (LDH) release were measured in PC12 cells induced with 200 μM CORT in the presence or absence of various concentrations of PBP for 48 h. Intracellular reactive oxygen species (ROS) generation, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and glutathione (GSH) content were examined to analyze the effect of PBP on CORT-induced oxidative stress. The levels of pro-inflammatory factors, the percentage of apoptotic cells, and apoptosis-related protein expression in PC12 cells were determined. PBP is mainly composed of protein subunits with molecular weights ranging from 1000 to 10,000 Da. PBP treatment increased cell viability and decreased the release of LDH in CORT-stimulated PC12 cells. Moreover, PBP reduced the level of CORT-induced oxidative stress by decreasing ROS levels and increasing SOD, GSH-Px activities and GSH content. PBP had an inhibitory effect on the CORT-induced inflammatory response through inhibition of the NF-κB signaling pathway. PBP also inhibited CORT-induced apoptosis by downregulating the mitochondrial apoptotic signaling pathway. These results suggest that PBP exerts a neuroprotective effect against CORT-induced cell injury by inhibiting oxidative stress, inflammation, and apoptosis. PBP could act as a neuroprotective agent against nerve injury induced by CORT. [ABSTRACT FROM AUTHOR]