ERK1/2 mediated inhibitory role of curcumin on STS-induced neurons toxic injury / 中国生化药物杂志

ABSTRACT

Objective To explore extracellular signal-regulated kinase ( ERK1/2 ) expression in the role of curcumin inhibited staurosporine (STS)-mediated neurons toxic injury through added PD098059, and to clarify ERK1/2 mediated inhibitory role of curcumin on STS-induced neurons toxic injury.Methods The neurons toxic injury model of primary cultured hippocampal neurons was established by STS.The experiment was divided into six groups:normal control group, STS model group, PD098059 +STS model group, curcumin +STS pretreatment group, curcumin+PD098059+STS treatment group and curcumin treatment group.The cell viability were determined by MTT method, lactate dehydrogenase (LDH) release rate, cell toxicity were detected, nuclear shape were observed by DAPI staining, and ERK1/2 expression were detected by Western blot method.Results The cell viability of curcumin +STS pretreatment group was significantly higher than STS model group ( P <0.001 ); the cell viability had no significant difference between PD098059 +STS model group and curcumin +PD098059 +STS treatment group;compared with curcumin +STS model group , the cell viability of curcumin +PD098059 +STS treatment group was significantly decreased ( P<0.001 ).LDH results showed that the nerve cell toxicity of curcumin +STS pretreatment group was obviously less than STS model group (P<0.001).The cell nuclear shape showed typical apoptosis morphological characteristics in STS model group, and curcumin inhibited the effect of STS mediated-neuronal apoptosis.ERK1/2 protein expression in curcumin +STS pretreatment group significantly increased compared with STS model group ( P <0.001 ) .Conclusion Curcumin inhibited STS-mediated neurons toxicity injury by up-regulating ERK1/2 expression.After PD098059 blocking the nerve cells ERK1/2 synthesis, the inhibitory action of curcumin failed to implemented, which illustrated that ERK1/2 mediated curcumin to inhibit STS-induced neuronal toxic injury.