CAJ | 학술논문

目的:探讨高温致畸中MAPKs激酶中的ERK1/2通路与JNK1/2通路蛋白表达及其作用,进一步揭示高温致畸机制.方法:在高温致金黄地鼠畸形的动物模型上,应用Western blotting技术检测对照组和高温组胚胎的丝裂原活化蛋白激酶ERK1/2及JNK1/2的表达及其磷酸化水平.结果:p-ERK1/2在对照组稳定表达;高温作用后p-ERK1/2表达与对照组相比活性降低,差异明显(P<0.05);p-JNK1/2在对照组不表达,在高温组各时段均出现表达,并于高温作用后16h活性达最大值,与对照组差异明显(P<0.05).结论:高温可导致胚胎MAPKs信号转导通路中p-ERK1/2活性表达降低、p-JNK1/2活性升高,引起胚胎发育过程中细胞增殖和凋亡的失衡,从而导致胚胎先天缺陷的发生,这可能是高温致畸的一条重要途径.
목적:탐토고온치기중MAPKs격매중적ERK1/2통로여JNK1/2통로단백표체급기작용,진일보게시고온치기궤제.방법:재고온치금황지서기형적동물모형상,응용Western blotting기술검측대조조화고온조배태적사렬원활화단백격매ERK1/2급JNK1/2적표체급기린산화수평.결과:p-ERK1/2재대조조은정표체;고온작용후p-ERK1/2표체여대조조상비활성강저,차이명현(P<0.05);p-JNK1/2재대조조불표체,재고온조각시단균출현표체,병우고온작용후16h활성체최대치,여대조조차이명현(P<0.05).결론:고온가도치배태MAPKs신호전도통로중p-ERK1/2활성표체강저、p-JNK1/2활성승고,인기배태발육과정중세포증식화조망적실형,종이도치배태선천결함적발생,저가능시고온치기적일조중요도경.
AIM: To study the expression and the role of ERK1/2 and JNK1/2 of MAPKs pathways in the development of neural tube defects induced by hyperthermia. METHODS: The animal models of golden hamster were produced by hyperthermia. The expression of ERK1/2 and JNK1/2, and levels of their phosphorylation were measured by Western blotting in control group and hyperthermia group. RESULTS: p-ERK1/2 steadily expressed in each control group, and the expression of p-ERK1/2 significantly decreased, which was different from that in the corresponding control group (P<0.05). The activity of p-JNK1/2 increased in hyperthermia group and the amount of p-JNK1/2 increased as compared to control group. The peak appeared at 16 h after exposed to hyperthermia (P<0.05). CONCLUSION: Hyperthermia, which induces a decrease in p-ERK1/2 expression and increases the expression of p-JNK1/2 of MAPKs pathway, results in the unbalance of cell proliferation and apoptosis, and induces neural tube defects.