N-乙酰半胱氨酸通过TRPC3介导钙离子通道对感染性早产小鼠的保护作用

Protective effect of N-acetylcysteine on TRPC3-mediated calcium channel of LPS-induced premature delivery mice

目的探讨N-乙酰半胱氨酸(NAC)在小鼠感染性早产中的作用机制,为临床先兆早产的预防及其药物靶向治疗的研发提供理论基础。方法建立LPS诱导的感染性早产小鼠模型,应用免疫组化、实时荧光定量PCR、Western blot检测孕鼠子宫组织中TRPC3的表达;实时荧光定量PCR、Western blot检测孕鼠子宫中Cav3.1和Cav3.2蛋白的表达。结果早产孕鼠离体子宫肌条肌张力明显增高,TRPC3高表达于早产小鼠子宫组织中,Cav3.1和Cav3.2蛋白在早产小鼠子宫中明显高表达,经NAC治疗后,TRPC3、Cav3.1和Cav3.2蛋白表达水平均下降。结论TRPC3与分娩的发动密切相关,NAC在感染性小鼠早产中通过降低TRPC3介导Cav3.1和Cav3.2蛋白发挥保护作用。

Objective To investigate the effect and possible mechanism of N-acetylcysteine（NAC）on mice with premature delivery to provide a theoretical basis for the prevention of clinical precursors and the development of drug targeted therapy.Methods LPS-induced mice premature delivery model was established.The expression of TRPC3 in the uterus of pregnant mice was detected by immunohistochemistry,quantitative real-time PCR and Western blot.The quantitative real-time PCR and Western blot were used to detect the expressions of Cav3.1 and Cav3.2 in the uterus of pregnant mice.Results The maternal muscle tension of the uterus was significantly increased,and the expression levels of TRPC3,Cav3.1 and Cav3.2 in the uterus were significantly higher in the premature mice than in normal mice.The treatment of NAC downregulated the expression levels of TRPC3,Cav3.1 and Cav3.2 proteins in the uterus significantly.Conclusion TRPC3 is related to the progression of the delivery,the protective effect of NAC on LPS-induced mice premature might be related to reducing the expression of TRPC3 mediated Cav3.1 and Cav3.2 signal molecules.