Physalin A exerts neuroprotective effects: inhibition of OGD/R-induced cellular pyroptosis and inflammatory responses in nerve cells

A prevalent cerebrovascular disease like the acute cerebral infarction is caused by cerebral thrombosis or arteriosclerosis that can result in ischemic necrosis of brain tissues. Treatment drugs of higher efficiency are required to be developed for acute cerebral infarction. Physalin A (PA) is a major compound from Physalis alkekengi L. and has pharmacological properties. However, the neuroprotective effects of PA are less reported and the mechanism remains unclear. The acute cerebral infarction cell model was constructed by treating PC12 cells with oxygen-glucose deprivation/reoxygenation (OGD/R). The impacts of PA on cell viability were determined by performing 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) releasing assays. Immunoblot and Enzyme-linked Immunosorbent assay (ELISA) were conducted to examine PA effects on inflammation. PA effects on pyroptosis were detected by performing immunoblot and immunostaining. Moreover, immunoblot was further conducted to confirm the mechanism. In this study, the survival and inhibition of the pyroptosis of OGD/R-induced PC12 cells were regulated by PA. Furthermore, PA suppressed the inflammation. PA inhibited mitogen-activated protein kinase (MAPK) pathway activation, and the activation of MAPK pathway reversed the neuroprotective effect of PA. Therefore, PA exerts neuroprotective effects by suppressing OGD/R-induced cellular pyroptosis and inflammatory responses in nerve cells.