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目的探讨新生大鼠脑白质损伤时GRP78和CHOP基因表达变化及意义。方法2日龄SD大鼠98只,实验组和对照组各49只,实验组大鼠制备脑白质损伤(WMD)动物模型,两组均于缺氧缺血后0、2、4、6、12、24 h及72 h处死,HE染色观察脑组织病理学变化,real time PCR技术检测GRP78mRNA及CHOPmRNA表达量变化。结果与对照组相比,实验组GRP78mRNA在缺氧缺血后2h表达开始上升,6 h达到峰值,缺氧缺血后2、4、6、12、24、72 h均增加(P<0.05)。实验组CHOPmRNA在缺氧缺血后2 h开始表达上调,逐渐上升,缺氧缺血后2、4、6、12、24、72 h均增加(P<0.05)。结论新生大鼠脑白质损伤时,实验组GRP78mRNA及CHOPmRNA表达较对照组显著升高,且两个基因表达升高有时序性。表明缺氧缺血导致内质网应激反应被激活,内质网应激可能是新生大鼠脑白质损伤的发病机制之一。
Objective To investigate the changes and significance of GRP78 and CHOP gene in white matter lesion of newborn rats. Methods Two-day-old SD rats (98 rats) were used in this study. The rats in the experimental group and the control group were each given 49 animals of experimental group with white matter damage (WMD). Both groups were subjected to 0,2,4,6, The rats were killed at 12, 24, and 72 hours. The pathological changes of brain tissue were observed by HE staining. The expression of GRP78 mRNA and CHOP mRNA were detected by real time PCR. Results Compared with the control group, the expression of GRP78mRNA in experimental group began to rise at 2h after hypoxia-ischemia and peaked at 6h, increased at 2, 4, 6, 12, 24 and 72 h after hypoxic-ischemia (P <0.05) . The expression of CHOP mRNA in experimental group began to increase at 2 h after hypoxic-ischemic insult, and gradually increased. Hypoxia-ischemia increased at 2, 4, 6, 12, 24 and 72 h (P <0.05). Conclusions The expression of GRP78mRNA and CHOPmRNA in the experimental group is significantly higher than that in the control group at the time of white matter damage in neonatal rats, and the expression of both genes is up-regulated. The results suggest that hypoxia and ischemia lead to the activation of endoplasmic reticulum stress. Endoplasmic reticulum stress may be one of the pathogenesis of white matter damage in neonatal rats.