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目的探讨p38MAPK蛋白激酶及Bax在高温致神经管畸形中的分子机制。方法将雌性金黄地鼠72只按完全随机设计分组法分为正常对照组和高温致神经管畸形实验组,每组36只。孕鼠于妊娠第8天进行高温水浴,并分别于高温后2、8、16、24、48、72h取出胚胎。Westernblot法对p38MAPK、P-p38MAPK及Bax活性进行分析。结果①Bax在正常对照组胚胎稳定表达,且无明显量的改变(P>0.05);Bax的表达在高温后8～48h明显升高,与正常对照组相比差异有统计学意义(P<0.05),于8、16h时表达增加最为显著(P<0.01)。②p38MAPK及P-p38MAPK在正常组中稳定低表达;而在高温致畸组中,p38MAPK的表达无明显变化(P>0.05),P-p38MAPK的表达在高温后8～48h均明显高于相应时间点的正常组(P<0.05),于16h时表达增加最为显著(P<0.01)。结论高温能促进p38MAPK蛋白激酶及其凋亡蛋白Bax的表达,诱发胚胎的细胞凋亡,导致神经管畸形的发生。
Objective To investigate the molecular mechanism of p38MAPK protein kinase and Bax in neural tube defects induced by hyperthermia. Methods 72 female Golden Hamster rats were randomly divided into normal control group and experimental group with high temperature induced neural tube defects, with 36 rats in each group. The pregnant rats were subjected to high temperature water bath on the 8th day of gestation, and the embryos were taken out at 2, 8, 16, 24, 48 and 72 h after the high temperature. Western blot analysis of p38MAPK, P-p38MAPK and Bax activity analysis. Results ① The expression of Bax was stable in the normal control group with no significant change (P> 0.05). The expression of Bax was significantly increased at 8 ~ 48 h after the hyperthermia, with significant difference compared with the normal control group (P <0.05 ), The expression increased most significantly at 8 and 16 h (P <0.01). ②The expression of p38MAPK and p-p38MAPK in stable group were lower than those in normal group (P> 0.05). However, the expression of p-p38MAPK was significantly higher than that in 8 ~ 48h after high temperature Point normal group (P <0.05), the expression increased most significantly at 16h (P <0.01). Conclusion High temperature can promote the expression of p38MAPK protein kinase and its apoptotic protein Bax, induce embryonic apoptosis and lead to the occurrence of neural tube defects.