[1]黄立宏 李刚 冯小芳等. 15d-PGJ2对糖尿病大鼠脑缺血再灌注损伤小胶质细胞活化及神经细胞凋亡的影响[J].卒中与神经疾病杂志,2016,23(03):149-153.[doi:10.3969/j.issn.1007-0478.2016.03.001]
　Huang Lihong,Li Gang,Feng Xiaofang,et al. Effect of 15d-PGJ2 on the activation of microglias and the apotosis of neurons after the injury of acute cerebral ischemia reperfusion in diabetic rats[J].Stroke and Nervous Diseases,2016,23(03):149-153.[doi:10.3969/j.issn.1007-0478.2016.03.001]
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 15d-PGJ2对糖尿病大鼠脑缺血再灌注损伤小胶质细胞活化及神经细胞凋亡的影响(/HTML)
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第23卷
期数:
2016年03期
页码:
149-153
栏目:
论 著
出版日期:
2016-06-24

文章信息/Info

Title:
 Effect of 15d-PGJ2 on the activation of microglias and the apotosis of neurons after the injury of acute cerebral ischemia reperfusion in diabetic rats
作者:
 黄立宏 李刚 冯小芳等
 200070 上海市闸北区中心医院神经内科(黄立宏 冯小芳 王罗军 杜洵昊); 上海同济大学东方医院神经内科(李刚)
Author(s):
Huang Lihong;  Li Gang;  Feng Xiaofang;  et al.
 Department of Neurology,ZhaBei Central Hospital,Shanghai 200070
关键词:
 ; 15d-PGJ2 凋亡 脑缺血 再灌注 糖尿病 小胶质细胞
Keywords:
 ; 15d-PGJ2 Apotosis Cerebral ischemia Reperfusion Diabetic Microglia
分类号:
R743
DOI:
10.3969/j.issn.1007-0478.2016.03.001
文献标志码:
A
摘要:
 目的 观察PPAR-γ激动剂15d-PGJ2对糖尿病脑缺血再灌注大鼠脑缺血再灌注损伤小胶质细胞活化及神经细胞凋亡的影响。方法 成年SD大鼠80只,随机分为4组:(1)假手术组;(2)正常血糖脑缺血组;(3)糖尿病脑缺血组;(4)糖尿病脑缺血+15d-PGJ2干预组。采用链脲佐菌素诱导糖尿病,应用改良的Zea-Longa法制作大鼠大脑中动脉闭塞再灌注模型。糖尿病脑缺血组+15d-PGJ2干预组在成功制备糖尿病大鼠模型后给予15d-PGJ2 200 μg·kg-1·d-1腹腔注射21 d后应用改良的Zea-Longa法制作大鼠大脑中动脉闭塞再灌注模型,再灌注后3 h腹腔注射15d-PGJ2 400 μg·kg-1,以后6 d每天给予15d-PGJ2 200μg·kg-1·d-1腹腔注射。每组分别于24 h、7 d各处死一批大鼠,并随机分为2组:一组行免疫组化法检测小胶质细胞CD68的表达水平及ELISA检测TNF-α与IL-1β水平,另一组用TUNEL法原位标记DNA片段检测凋亡细胞计数。结果 正常血糖脑缺血组、糖尿病脑缺血组、糖尿病脑缺血+15d-PGJ2干预组与假手术组比较,再灌注24 h、再灌注7 d CD68阳性面积、TNF-α与IL-1β水平、神经细胞凋亡率均明显增加(P<0.05); 糖尿病脑缺血组在再灌注24 h、再灌注7 d CD68阳性面积、TNF-α与IL-1β水平、神经细胞凋亡率明显高于正常血糖脑缺血组(P<0.05); 糖尿病脑缺血+15d-PGJ2干预组再灌注24 h、再灌注7 d CD68阳性面积、TNF-α与IL-1β水平、神经细胞凋亡率低于未干预组(P<0.05)。结论 糖尿病脑缺血组与正常血糖脑缺血组相比较CD68阳性面积更大、TNF-α与IL-1β水平更高及神经细胞凋亡率更高; 15d-PGJ2可减少糖尿病脑缺血大鼠小胶质细胞激活、减少炎症因子分泌、降低神经细胞凋亡率。
Abstract:
 ObjectiveTo investigate the effect of PPAR-γ agonist 15d-PGJ2 on the activation of microglias and the apotosis of neurons after acute cerebral ischemia reperfusion in diabetic rats.Methods 80 adult SD rats were randomly divided into four groups:(1)sham group;(2)normal blood glucose of cerebral ischemia group;(3)diabetic cerebral ischemia group;(4)diabetic cerebral ischemia and 15d-PGJ2 intervention group. Induce Diabetic with streptozotoci, use modified Zea-longa method to set up rat middle cerebral artery occlusion model after successful preparing diabetic rats.The diabetic cerebral ischemia group and 15d-PGJ2 intervention group received 15d-PGJ2200 μg·kg-1·d-1 intraperitoneal injection in 21 days,then set up middle cerebral artery occlusionmodel with a modified Zea-longa method,3 hours after reperfusion 15d-PGJ2 400 μg·kg-1·d-1intraperitoneal injection was given,and 15d-PGJ2 200 μg/kg/d intraperitoneal injection was given in later 6 days.The rats were killed at24 h,7day, and randomly divided into two groups:one group, the expression of microglias and the content of TNF-α,IL-1β was detected with immunohistochemical method, another group,apotosis of neurons was detected with TUNEL.Results Compare to the sham group, the positive area of CD68、the content of TNF-α,IL-1β、 the apotosis ratio of neurons in the other three groups24 hours and 7 days after reperfusion were higher.(P<0.05); the positive area of CD68、the content of TNF-α,IL-1β、the apotosis ratio of neurons in diabetic cerebral ischemia group in 24 hours and 7 days after reperfusion were higher than that in normal bloodglucose of cerebral ischemia group(P<0.05); the positive area of CD68、the content of TNF-α,IL-1β、the apotosis ratio ofneurons in diabetic cerebral ischemia and 15d-PGJ2 intervention in 24 hours and 7 days after reperfusion group were lower than that in diabetic cerebral ischemia group(P<0.05).Conclusion Compare to normal blood glucose of cerebral ischemia group,the positive area of CD68,the content of TNF-α,IL-1β,the apotosis ratio of neurons in the diabetic cerebral ischemia group were higher, 15d-PGJ2 can reduce activation of microglias, secretion of inflammatory cytokines and the ratio of neuron apotosis.

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备注/Memo

备注/Memo:
 (2015-09-14收稿 2015-11-19修回)
更新日期/Last Update: 2016-06-24