The Protective Effect Of Helicid On Corticosterone Induced Injury In PC12 Cells Through ERK1/2 Signaling Pathway

Objective This study aimed to examine the protective effects of Helicid on corticosterone-induced neurotoxicity and its possible mechanisms,using PC12 cells as a suitable in vitro model of depression.Methods In this paper,PC12 cells were treated with 600 μM of corticosterone in the absence or presence of Helicid in varying concentrations for 24 h.Then,cell viability was measured by CCK-8 assay.There released amount of lactate dehydrogenase(LDH)was quantified using LDH assay kit.Apoptosis of PC12 cells were measured by Hoechst33342 and flow cytometer assays.In addition,Helicid co-treatment was found to reverse the decreased brain-derived neurotrophic factor(BDNF)mRNA level caused by corticosterone in PC12 cells.Pretreatments with ERK1/2 pathway inhibitors were used to investigate the possible pathways involved in the protection of Helicid.The phosphorylation of ERK was analyzed byWestern blot.Results The results showed that treatment with 600 μM of corticosterone could induce cytotoxicity in PC12 cells.However,different concentrations of Helicid(25 μM,50 μM,100 μM)significantly increased the cellviability,decreased the LDH release and upregulate the BDNF mRNA expression.The protective effect of Helicid was reversed by U0126.Western blot analyses showed that Helicid induced the phosphorylation of ERK by the ERK1/2 pathway and reversed the reduction of the phosphorylated ERK induced by corticosterone.Conclusion: Helicid protects PC12 cells against corticosterone-induced cell death by modulating the activity of the ERK1/2 pathway.