摘要
目的探讨缺血后处理(I-Post)对糖尿病大鼠局灶性脑缺血再灌注(I/R)损伤的影响。方法采用链脲佐菌(STZ)腹腔注射方式建立糖尿病大鼠模型,将制模成功的糖尿病大鼠随机分为4组,即空白对照组、假手术组、缺血再灌注组(I/R组)及缺血后处理组(I-Post组)。I/R组及I-Post组均通过线栓法制作大鼠大脑中动脉阻塞(MCAO)模型,并且I-Post组于大脑中动脉阻塞90min后,反复进行3次短暂再灌注干预(灌注15S后缺血15s);假手术组手术步骤同上,但不插入线栓;空白对照组不给予任何处理。于缺血90min、再灌注6h后对所有大鼠进行神经功能评分(NDS)、脑梗死体积测定、观察脑组织神经细胞形态学变化及计数TUNEL阳性凋亡细胞数量。结果I-Post组与I/R组比较,其神经功能评分组间差异无统计学意义(P〉0.05),I-Post组大鼠脑梗死体积及凋亡细胞数量均较I/R组明显减小(P〈0.05)。结论I-Post处理能抑制糖尿病脑缺血大鼠神经细胞凋亡,减轻局灶性I/R损伤。
Objective To observe the effect of ischemic postconditioning on cerebral ischemia-reperfusion (I/R) injury in diabetic rats. Methods A rat model of diabetes was established using a single intraperitoneal injection of streptozotocin in 40 male Sprague-Dawley rats. Focal ischemia was induced by transient middle cerebral artery occlusion (MCAO) using a thread. The rats were randomly assigned to a control group, a sham-operated group, an I/R group and an I-Post group. The animals in the I/R group were subjected to MCAO for 90 min and then reperfusion. Those in the I-post group were subjected to MCAO and 3 cycles of transient ischemia-reperfusion ( 15 seconds ischemia then 15 seconds reperfusion) before persistent reperfusion. Neurological deficit scores, infarct volume, histological changes in the brain and the number of apoptotic ceils were measured 6 hours later. Results There was no significant difference in neurological deficit scores between the I/R group and the I-post group. The histological chan- ges and apoptotic ceils were significantly less in the I-post group compared with the I/R group. Conclusion Ischemic postconditioning can inhibit cell apoptosis and reduce cerebral I/R injury after focal cerebral ischemia-reperfusion in diabetic rats.
出处
《中华物理医学与康复杂志》
CAS
CSCD
北大核心
2008年第5期316-319,共4页
Chinese Journal of Physical Medicine and Rehabilitation
基金
山东省自然科学基金资助项目(Y2007C087)
关键词
缺血后处理
脑缺血
再灌注损伤
细胞凋亡
糖尿病
Ischemic postconditioning
Cerebral isehemia
Reperfusion injury
Cell apoptosis
Diabetes mellitus