Calcium facilitates NLRP3 inflammasome-induced oxidative stress in SHSY5Y cells / 中华行为医学与脑科学杂志

ABSTRACT

Objective To study calcium chelator BAPTA-AM antagonize the cellular oxidative stress induced by hydrogen peroxide ( H2 O2 ) and to explore the effect of calcium ion on the cell degeneration mediated by NLRP3.Methods The SHSY5Y cell model of oxidative stress was made by hydrogen perox-ide,then the cell model was treated with calcium ion carrier A23187 or BAPTA-AM,a higher efficiency cal-cium chelating agent.The cells were divided into 4 groupsH2O2 treatment group,H2O2+A23187 group, H2 O2+A23187 +BAPTA-AM group and control group.NLRP3 protein was detected by Western blot,and Caspase-1 and IL-1βwere detected by ELISA.Results NLRP3 expression was significantly increased in cells treated by hydrogen peroxide(P<0.05) .The NLRP3 protein continued to increase, and the expression of Caspase-1((57.1±19.2)pmol/L) and IL-1β((484.2±49.5)pg/ml) protein was also increased signifi-cantly in cells treated by A23187,and the difference had statistically significant for caspase-1 or IL-1βin H2O2+A23187 group compared with those in control group(Caspase-1(26.8±12.9)pmol/L,IL-1β(326.9 ±52.1) pg/ml) (P<0.05, P<0.01) .NLRP3,Caspase-1 and IL-1βwere all significantly reduced after adding a high-er efficiency calcium chelating agent BAPTA-AM.Conclusion Calcium overload is likely to enhance the oxidative stress induced by hydrogen peroxide and engender neurodegeneration mediated by NLRP3 inflammasome.