超负荷血糖对鼠局灶性脑缺血侧皮质内皮抑素表达的影响

The effects of hyperglycemia on expression of endostatin in focal cerebral ischemia injury of rats

目的观察超负荷血糖对鼠局灶性脑缺血侧皮质区内皮抑素(endostatin)表达的影响,进一步探讨超负荷血糖加重脑缺血损伤的分子机制。方法用SD大鼠腹腔内注射链脲佐菌素首先建立糖尿病高血糖大鼠模型,继而应用栓线法建立永久性局灶性脑缺血模型。随机分为3大组:假手术组、脑缺血组和糖尿病脑缺血组。于缺血24h时间点行神经功能评分、TTC染色测梗死面积、TUNEL法检测细胞凋亡数目、免疫组化及Western blot检测ES表达,并进行图像分析。结果糖尿病脑缺血组的神经功能评分为(4.73±0.35)、梗死面积为(50.12±3.54)、细胞凋亡数为(26.22±2.35)、免疫组化检测ES为(99.35±3.25)及Western blot检测ES为(1.193±0.045)。脑缺血组的神经功能评分为(3.18±0.65)、梗死面积为(39.98±2.02)、细胞凋亡数为(17.28±1.01)、免疫组化检测ES为(113.17±1.35)及Western blot检测ES为(1.033±0.032)。与脑缺血组相比,糖尿病脑缺血组的神经功能评分、梗死面积、细胞凋亡数、ES蛋白表达均明显增加(P<0.05)。结论血管再生可能参与了超负荷血糖加重脑缺血损伤的过程,上调ES表达可能是超负荷血糖加重脑缺血损伤的机制之一。

Objective To study the effects of hyperglycemia on expression of endostatin（ES） in ischemic penumbra after cerebral ischemia of rats.Methods Hyperglycemia model was made by injection of streptozocin through abdomen in rats,and focal cerebral ischemia model was made by occluding the middle cerebral artery with nylon line in streptozocin-induced hyperglycemic rats and then the scores of neurological deficit,infarct volume as well as apoptotic neurons were estimated.In addition,immunohistochemistry（IHC） and Western-blot（WB） were used to detect the expression level of ES in adult male Sprague-Dawley rats.Results The scores of neurological deficite,the infarct volum as well as the number of apoptotic neurons were higher siginificantly in hyperglycemic rats than which of nonhyperglycemic rats.The same things happened in the expression of ES in the groups of hyperglycemic rats and nonhyperglycemic rats.Conclusion Angiogenesis may play an important roles in that hyperglycemia aggravating cerebral ischmia injury,and hyperglycemia could aggravate cerebral ischemia injury by increasing the expression of ES.