Sodium hydrogen sulfide supplementation with exogenous H2S improves neurological dysfunction in offspring autistic mice
Objective:Exploring the supplementation of exogenous loydrogen sulfide(H2S)with sodium hydro-gen sulfide(NaHS)while upregulating 3-mercaptopyruvate sulfurtransferase(MPST)and cystathionine β-synthase(CBS),promoting endogenous H2 S production,and jointly improving neurological dysfunction in autism spectrum disorders(ASDs)mice.Methods:Fifteen C57BL/6 pregnant mice were randomly divided into a normal control group(Con group,n=3),a valproic acid model group(VPA group,n=4),a NaHS intervention group(VPA+NaHS group,n=4),and a normal asaline control group(VPA+NS group,n=4).Except for the Con group,the offspring autism models were prepared by intraperitoneal injection of 300 mg/kg VP A in the other three groups of 12 d pregnant mice.The NaHS+VPA group and NS+VPA group were orally administered evevyday to pregnant mice starting from day 13 of pregnancy 100 μmol/kg NaHS until weaning of offspring mice at 23 days.Fifteen male offspring of the four groups were selected for behavioral testing(elevated cross test,open field test,and stereotyped behavior observa-tion)to identify the model and treatment effect.Use H2S assay kit to detect the concentration of H2S in the striatum,use Western blot to detect the expression of H2S related molecules MPST and CBS,and use TUNEL assay kit to detect neuronal apoptosis.Results:Compared with the Con group,the VP A induced ASDs model significantly increased neurological dysfunc-tion in mice(P＜0.01),decreased the expression of MPST and CBS in neurons of striatum,and promoted cell apoptosis(all P＜0.05).Conversely,NaHS significantly improve neurological dysfunction(P＜0.05),increase endogenous H2 S genera-tion(all P＜0.05)by promoting the expression of MPST and CBS,and inhibit neuronal apoptosis(P＜0.05).Conclusion:NaHS not only increase exogenous H2S through enhancing the expression of molecules related to H2S generation,but also inhibit neuronal apoptosis,and effectively improve neurological dysfunction in ASDs mice.
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