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作 者:林冬融[1] 揭育东 韩江全[1] Lin Dongrong;Jie Yudong;Han Jiangquan(Department of Neurology,The Fifth Affiliated(Zhuhai)Hospital of Zunyi Medical University,Zhuhai Guang-dong 519100,China;Department of Emergency,The Fifth Affiliated(Zhuhai)Hospital of Zunyi Medical University,Zhuhai Guangdong 519100,China)
机构地区:[1]遵义医学院第五附属(珠海)医院神经内科,广东珠海519100 [2]遵义医学院第五附属(珠海)医院急诊科,广东珠海519100
出 处:《遵义医学院学报》2018年第4期424-430,共7页Journal of Zunyi Medical University
基 金:珠海市医学科研基金资助项目(NO:2017J028)
摘 要:目的对尤瑞克林(urokallikrein)干预糖尿病大鼠局灶性脑缺血再灌注损伤后细胞色素C(Cytochrome-C,Cyt-C)及半胱氨酸天冬氨酸蛋白酶-3(cysteinylaspartate specific proteinase-3,caspase-3)表达的变化进行观察,探讨尤瑞克林对糖尿病合并急性脑缺血再灌注损伤神经细胞的保护机制。方法 82只雄性Sprague-Dawley(SD)大鼠随机分为3大组:假手术组10只,缺血组36只,尤瑞克林组36只。以无菌链脲佐菌素(streptozotocin,STZ)腹腔注射制作糖尿病大鼠模型,继而制作大脑中动脉闭塞再灌注(MCAO/R)模型。采用Bederson评分标准进行神经功能评分,原位缺口末端标记法(TUNEL法)检测细胞凋亡数目,免疫组织化学染色法检测Cyt-C及caspase-3表达。结果①尤瑞克林组的神经功能评分在各再灌注时间点均低于缺血组;②尤瑞克林组的凋亡细胞数在各再灌注时间点均少于缺血组;③尤瑞克林组的Cyt-C及caspase-3表达在各再灌注时间点均低于缺血组。结论尤瑞克林对糖尿病大鼠局灶性脑缺血再灌注后神经细胞凋亡的抑制作用可能是通过下调Cyt-C及caspase-3的表达而实现。Objective To observe the effect of urokallikrein on the expressions of Cytochrome-C and caspase-3 in diabetes rats with focal cerebral ischemia-reperfusion injury and further to explore the mechanism of urokallikrein in protecting cerebral infarction with diabetes. Methods The 82 adult male Sprague-Dawley(SD) rats were divided randomly into 3 groups: the sham-operation group(10 rats),the cerebral-ischemia group(36 rats) and the urokallikrein group(36 rats). Diabetes model was made by injection of streptozotocin through abdomen in rats and focal cerebral ischemia-reperfusion injury was made by occluding the middle cerebral artery.Neurological deficits were estimated with the Bederson Scale. The apoptotic neurons were stained with the terminal-deoxynucleotidyl transferase mediated d UTP nick end labeling(TUNEL). The expressions of Cyt-C and caspase-3 were detected with immunohistochemistry. Results(1) The neurological deficit score in urokallikrein group was lower than that in cerebral-ischemia group at the same reperfusion time.(2) The number of apoptotic neurons in urokallikrein group was lower than that in cerebral-ischemia group at the same reperfusion time.(3)Compared with cerebral-ischemia group at the same reperfusion time,the expressions of Cyt-C and caspase-3 in urokallikrein group were much lower. Conclusion Urokallikrein may protect diabetes rats from neurons apoptosis after focal cerebral ischemia-reperfusion by inhibiting the expressions of Cyt-C and Caspase-3.
关 键 词:尤瑞克林 糖尿病 脑缺血再灌注 细胞色素C 半胱氨酸天冬氨酸蛋白酶-3
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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