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目的探讨高温致畸MAPKs中JNK1/2通路蛋白及凋亡基因Caspase-3的表达作用及其机理。方法孕鼠于受精第8天置42℃水浴,持续20min后,分别于2、8、16、24、48、72h经麻醉处死剖腹取胎,并分为高温组(2～72h,42℃)和对照组(2～72h,37℃)。采用Westernblot技术检测JNK1/2、P-JNK1/2及Caspase-3的表达量。结果高温组JNK1/2的表达量与对照组无明显差异,各组内不同时间的表达量无明显变化;P-JNK1/2在对照组中不表达,高温组8～48h时的表达量均高于相应的对照组(P<0.05),于16h时表达增加最为显著;Caspase-3在对照组中无表达,在高温组8～48h时表达增加(P<0.05),于8h时增加最为显著。结论高温刺激能促使JNK1/2发生磷酸化和凋亡基因Caspase-3的活化,这可能是高温致胚胎先天性畸形的原因之一。
Objective To investigate the expression of JNK1 / 2 pathway protein and apoptosis gene Caspase-3 in hyperthermic teratogenic MAPKs and its mechanism. Methods The pregnant rats were placed in water bath at 42 ℃ on the 8th day of fertilization and continued for 20 minutes. The pregnant rats were anesthetized and killed at 2, 8, 16, 24, 48, and 72 hours respectively and were divided into high temperature group (2-72h, 42 ℃) And control group (2 ~ 72h, 37 ℃). The expression of JNK1 / 2, P-JNK1 / 2 and Caspase-3 were detected by Western blot. Results There was no significant difference in the expression of JNK1 / 2 between the high temperature group and the control group. The expression of JNK1 / 2 in the high temperature group did not change significantly at different time points. The expression of P-JNK1 / 2 was not observed in the control group (P <0.05), and the expression of Caspase-3 was the highest at 16h. The expression of Caspase-3 was not increased in the control group at 8 ~ 48h (P <0.05) Significant. Conclusion High-temperature stimulation can induce phosphorylation of JNK1 / 2 and activation of Caspase-3, which may be one of the causes of congenital malformation of embryos.