摘要
目的研究大鼠局灶性脑缺血-再灌注(IR)后脑组织X-连锁凋亡抑制蛋白(X-linked inh ib itor of apoptosis prote in,X IAP)和Caspase-3 p17的动态表达。方法30只雄性W istar大鼠,分为假手术组、缺血1.5 h后再灌注6、12、24、48和72 h组,每组5只。采用线栓法制作局灶性脑缺血1.5 h再灌注动物模型。用免疫组化法分别观察脑组织X IAP、Caspase-3 p17表达。结果假手术组和IR组非缺血侧可见少量X IAP阳性细胞,但未见Caspase-3 p17阳性细胞;与假手术组相比,X IAP阳性细胞再灌注6 h开始增加(P=0.00),12 h达高峰,24 h下降,48 h趋于正常(P=0.549);而再灌注6 h可见少量Caspase-3 p17阳性细胞,24 h达到高峰,至72 h仍较多,显著高于再灌注6 h时(P=0.004)。结论局灶性脑缺血可诱导凋亡抑制蛋白X IAP和促凋亡蛋白Caspase-3 p17短暂性表达增加,且前者表达的高峰时间早于后者。
Objective To study the dynamic expression of X-linked inhibitor of apoptosis protein （XIAP） and caspase-3 p17 after ischemia/reperfusion （IR） in rates, Methods Thirty male Wistar rats were divided into sham-operated, ischemia 1, 5 hours and reperfusion for 6, 12, 24, 48 and 72 hours （ n = 5 in each group）, A model of reperfusion after 1.5 hours of focal cerebral ischemia was established with the suture method, The expression of XIAP and caspase-3p17 in brains were observed respectively by immuno- histochemical method. Results A small amount of XIAP- positive cells were observed in the non-ischemic side in the sham-operated and IR groups, but no caspase-3 p17 positive cells were observed. The XIAPpositive cells expression began to increase （ P = 0. 00） at 6-hour reperfusion, it reached to the peak at 12 hours and began to decrease at 24 hours, and then it gradually returned to normal at 48 hours （P= 0. 549 ） as compared with the sham-operated group; a small amount of caspase-3 p17 positive cells were observed at 6-hour reperfusion, they reached the peak at 24 hours and remained for 72 hours, and they were significantly more than those at 6 hours after reperfusion （ P = 0, 004 ）, Conclusion Focal cerebral ischemia may induce the expression of apoptosis-inhibiting gene XIAP and apoptosis-promoting gene caspase- 3 p17 to increase transiently, and the peak time of the former expression is earlier than that of the latter.
出处
《中国脑血管病杂志》
CAS
2006年第7期317-321,共5页
Chinese Journal of Cerebrovascular Diseases
基金
广西自然科学基金资助(桂科自0542091)
