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目的探讨沙鼠脑缺血再灌注损伤后脑组织中Hsp22和c-fos的表达变化及相应的保护机制。方法健康雄性蒙古沙鼠制作脑缺血再灌注模型,缺血10 min,再灌注6 h、1、3、7 d。采用HE染色、免疫组织化学染色法观察脑组织的病理变化,Hsp22和c-fos的表达情况。结果 (1)HE染色:脑缺血再灌注组根据时间点的不同可见胶质细胞增生、肥大,细胞间质和细胞水肿,神经元坏死;(2)免疫组化:缺血再灌注损伤后Hsp22的表达上调,于第3 d达到高峰,与对照组比较有显著差异(p<0.05),第7 d开始下降但仍高于正常组和假手术组;c-fos在脑缺血再灌注后表达明显增高,于第1 d达到高峰,与对照组比较有显著差异(p<0.05),随后逐渐减少。结论沙鼠脑缺血再灌注后脑组织Hsp22及c-fos表达上调,推测Hsp22可能通过抑制c-fos的活性而起到凋亡负性调节的作用。
Objective To investigate the expression of Hsp22 and c-fos in brain tissue of gerbil after cerebral ischemia-reperfusion injury and the corresponding protective mechanism. Methods Healthy male Mongolians gerbils were used to make cerebral ischemia-reperfusion model. The models were ischemia 10 min, reperfusion 6 h, 1, 3, 7 d. The pathological changes of brain tissue and the expression of Hsp22 and c-fos were observed by HE staining and immunohistochemical staining. Results (1) HE staining: According to the time point, the glial cell proliferation, hypertrophy, interstitial cells and edema and neuron necrosis were observed; (2) Immunohistochemistry: After ischemia-reperfusion injury The expression of Hsp22 was up-regulated on the 3rd day, which was significantly higher than that of the control group (p <0.05), but decreased on the 7th day but still higher than that of the normal group and the sham operation group The expression was significantly increased at 1 d, which was significantly different from that of the control group (p <0.05), and then decreased gradually. Conclusion The expression of Hsp22 and c-fos in brain tissue of gerbils after cerebral ischemia-reperfusion is up-regulated. It is speculated that Hsp22 may play a negative regulatory role by inhibiting the activity of c-fos.