MAPKS在高温致金黄地鼠神经管畸形中的表达及其意义研究
摘要
目的:研究MAPKS信号传导通路在高温致金黄地鼠神经管畸形中的表达及其意义研究。方法:选取健康成熟的金黄地鼠,通过孕第8天下午15-16时进行水浴其腹部(水温42℃,时间20分钟)建立高温致神经管畸形的动物模型。肉眼及解剖显微镜下观察胚鼠的畸形情况。应用免疫组织化学的方法检测MAPKS信号传导通路中的P-ERK1/2.P-JNK1/2,P-P38在胚鼠的不同发育阶段,内介膜、神经管上皮、脊索与神经管周围的间质中表达量的变化。并分析3个磷酸化蛋白的功能。在高温导致神经管中所起的作用。结果:在高沮处理后的各期胚胎的上述结构中,P-ERK1/2、P-JNK1/2、P-P38的免疫组织化学染色均明显减弱,不同发育阶段及不同结构的着色强度也不同,特别是P-JNK,对照组中9、10、11的阳性率分别为95%、55%、20%,而实验组中P-JNK的阳性率分别为52%、24%、6%,两组比较,在第9、10天,P-JNK的阳性表达率有统计学意义,说明.P-JNK1/2, P-ERK1/2,P-P38在高温致神经管崎形中有重要作用,特别是JNK的表达意义更大。结论:MAPK信号传导系统对高温导致的神经管畸形中有一定促进作用。
Objective:The Present experiment aims to build NTDs golden hamsters model induced by hyperthermia and sudy the role of MAPKS in neural tube defects ,and therefore to explore the possible mechanism in hyperthermia inducd the neural tube defects .Method : The experimental animals were immersed in water bath at 42C and the contol animal did nothing.The embryos of the animals in the both groups were removed respectively at24,48 and 96h after immersion. The sections of each group were stained with immunohistochemical ABC method for observation of loealization distribution and changes of P-JNK, P-ERK, P-P38 in the neural epithelium and the innermembrane,the notochord and the mesenehyme around the neural tube.Result: The results showed that P-JNK, P-ERK, P-P38 immunoreactivity occurred widely in the normal embryonie neural epithelium and its basement membrane.notochord and mesenchy tne around the neural tube , and the immunoreactivity of P-JNK,P-ERK,P-P38decreased gradually with embryonic age the stain intensity for P-JNK,P-ERK,P-P38 in each treated group became remarkable weaker than that in the control group. the expression rates of p-jnk in 9,10,11 in the control group respectivelly is95%,55%,20%.but in treated group , the expression rates of p-jnk in 9,10,11 respectivelly is 52%,24%,6%.In 9,10.the expression rates of P-JNK have differentiation.Conclusions: The above results suggest that P-JNK, P-ERK,P-P38 is an important neurotrophic factor for the developrnent of neural tube.Hyperthermia can reduce P-JNK, P-ERK, P-P38 in the embyonie struetures above mentioned,which maybe a contributory factor for neural tube defects.
Objective:The Present experiment aims to build NTDs golden hamsters model induced by hyperthermia and sudy the role of MAPKS in neural tube defects ,and therefore to explore the possible mechanism in hyperthermia inducd the neural tube defects .Method : The experimental animals were immersed in water bath at 42C and the contol animal did nothing.The embryos of the animals in the both groups were removed respectively at24,48 and 96h after immersion. The sections of each group were stained with immunohistochemical ABC method for observation of loealization distribution and changes of P-JNK, P-ERK, P-P38 in the neural epithelium and the innermembrane,the notochord and the mesenehyme around the neural tube.Result: The results showed that P-JNK, P-ERK, P-P38 immunoreactivity occurred widely in the normal embryonie neural epithelium and its basement membrane.notochord and mesenchy tne around the neural tube , and the immunoreactivity of P-JNK,P-ERK,P-P38decreased gradually with embryonic age the stain intensity for P-JNK,P-ERK,P-P38 in each treated group became remarkable weaker than that in the control group. the expression rates of p-jnk in 9,10,11 in the control group respectivelly is95%,55%,20%.but in treated group , the expression rates of p-jnk in 9,10,11 respectivelly is 52%,24%,6%.In 9,10.the expression rates of P-JNK have differentiation.Conclusions: The above results suggest that P-JNK, P-ERK,P-P38 is an important neurotrophic factor for the developrnent of neural tube.Hyperthermia can reduce P-JNK, P-ERK, P-P38 in the embyonie struetures above mentioned,which maybe a contributory factor for neural tube defects.
引文
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