| 刘 恋,夏中元,袁 泉,赵 博,江 梦.后处理对心肌缺血再灌注致脑损伤中炎症因子及GFAP的影响[J].现代生物医学进展英文版,2017,17(27):5206-5209. |
| 后处理对心肌缺血再灌注致脑损伤中炎症因子及GFAP的影响 |
| Effect of Post-conditioning in Brain Injury Induced by Myocardial IR on Inflammatory Factor and GFAP |
| Received:January 30, 2017 Revised:February 25, 2017 |
| DOI：10.13241/j.cnki.pmb.2017.27.002 |
| 中文关键词: 缺血后处理 心肌缺血再灌注 炎症因子 胶质纤维酸性蛋白 |
| 英文关键词: Post-conditioning Myocardial ischemia reperfusion Inflammatory factor GFAP |
| 基金项目:湖北省自然科学基金项目(2016CFB167)；中央高校基本科研业务费专项基金项目(2042017kf0147) |
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| 中文摘要: |
| 摘要 目的：探讨缺血后处理对心肌缺血再灌注致脑损伤中炎症因子及胶质纤维酸性蛋白的影响。方法：24只雄性SD大鼠随机分为3组(n=8)，假手术组(Sham)、心肌缺血/再灌注组(IR)、后处理组(IPost)。结扎大鼠冠状动脉左前降支30 min，复流120 min建立大鼠心肌缺血/再灌注模型。后处理组于再灌注前进行缺血后处理，再灌注10 s，缺血10 s，共3次。断头处死大鼠取脑组织，光镜下观察病理学结果，Western blot检测炎性因子IL-6、IL-8、IL-10，免疫组化法检测GFAP。结果：与Sham组相比较，IR组脑组织炎症因子IL-6，IL-8表达增加，IL-10下降(P<0.01)，而后处理可以降低脑组织中IL-6，IL-8的表达，增加IL-10的表达(P<0.01)；与Sham组相比较，IR组脑组织GFAP表达增多(P<0.05)，而后处理可以显著增加脑组织中GFAP的表达(P<0.01)。结论：心肌缺血后处理可以减少脑组织中炎症因子的表达，增加GFAP的表达，从而起到脑保护作用。 |
| 英文摘要: |
| ABSTRACT Objective: To evaluate the effect of post-conditioning in brain injury induced by myocardial I/R on inflammatory factor and GFAP. Methods: Male Sprague-Dawley rats were randomly allocated into 3 groups (n=8): group Sham, group IR, group IPost. Myo- cardial IR was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min. group IPost received 3 cy- cles of 10 s reperfusion followed by 10 s ischemia at the end of myocardial ischemia. The rats were sacrificed at 120 min of reperfusion and the brains were removed for microscopic examination, inflammatory factors and GFAP. Results: Compared with group Sham, IL-6, IL-8 were significantly increased, IL-10 was down-regulated in group IR(P<0.01). Post-conditioning can decrease IL-6, IL-8 and up-regu- lated IL-10(P<0.01). When compared with group Sham, the expression of GFAP was higher in group IR(P<0.05), however, the GFAP in group IPost is the most among these three groups(P<0.01). Conclusion: Post-conditioning could protect brain by decreasing inflammatory factors, increasing GFAP, which both from brain injury induced by myocardial ischemia reperfusion. |
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