LAUSR

Bupivacain, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Paeoniflorin has been widely reported as a potential neuroprotective agent in neural injury models. However, the roles and molecular basis of paeoniflorin in bupivacaine‐induced neurotoxicity are still undefined. In the current study, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay was performed to detect cell viability. Apoptotic rate was measured through double‐staining of Annexin V‐FITC and propidium iodide on a flow cytometer. Western blot assay was carried out to examine the protein levels of p38 mitogen‐activated protein kinase (p38 MAPK), phosphorylated‐p38 MAPK (p‐p38 MAPK), Bcl‐2, and Bax. caspase‐3 activity was determined using a caspase‐3 activity assay kit. We found that paeoniflorin dose‐dependently attenuated bupivacaine‐induced viability inhibition and apoptosis in SH‐SY5Y cells. Moreover, paeoniflorin inhibited bupivacaine‐induced activation of p38 MAPK pathway in SH‐SY5Y cells. Paeoniflorin alone showed no significant effect on cell viability, apoptosis and p38 MAPK signaling in SH‐SY5Y cells. Inhibition of p38 MAPK signaling by SB203580 or small interfering RNA targeting p38 (si‐p38) abated bupivacaine‐induced viability inhibition and apoptosis in SH‐SY5Y cells. In conclusion, paeoniflorin alleviated bupivacaine‐induced neurotoxicity in SH‐SY5Y cells via suppression of the p38 MAPK pathway, highlighting the potential values of paeoniflorin in relieving bupivacaine‐induced neurotoxicity.