G蛋白偶联受体17对脑缺血损伤大鼠iNOs、TNF-α表达的影响
Effects of GPR17 on iNOs and TNF-α expression during ischemic brain injury
目的 观察G蛋白偶联受体17(GPR17)对脑缺血损伤炎症介质iNOs、TNF-a表达的影响。方法 健康雄性Sprague-Dawley大鼠随机分为对照组、模型组、NC组与GPR17 siRNA组。大鼠侧脑室埋管,以RNA干扰技术,靶向沉默脑内GPR17表达。以线栓法制备大鼠局灶性脑缺血模型,采用免疫组化方法检测炎症介质iNOs、TNF-α的表达。结果 脑缺血复灌24小时模型组出现明显的梗死灶,与对照组比较,模型组缺血区iNOs、TNF-α的表达显著上调 (P <0.01)。与模型组比较,GPR17干预显著减轻脑缺血复灌24小时损伤,抑制缺血区iNOs、TNF-α的表达 (P <0.01)。结论 GPR17 siRNA减轻脑缺血损伤,抑制缺血区炎症介质表达。
Objective To observe the effect of G protein coupled receptor 17 (GPR17) on the expression of inducible nitric oxide synthase (iNOs) and tumor necrosis factor-α (TNF-α) during cerebral ischemic injury. Method Male Sprague-Dawley rats were randomly divided into 4 groups: control group, saline group, NC group and GPR17 siRNA group. Because no GPR17 selective antagonist is currently available, RNA interference strategy was used in vivo to evaluate the regulatory role of GPR17. Ischemic brain injury was induced by middle cerebral arterial occlusion (MCAO) methods. The expression of iNOs and TNF-α was detected by immunohistochemistry, respectively. Results Compared with the control group, the expression of iNOs and TNF-α in the ischemic area were significantly elevated (P <0.01). Compared with the saline group, GPR17 intervention significantly reduced the cerebral ischemia injury, and inhibited the increased expression of iNOs and TNF-α in ischemic area (P <0.01). Conclusion GPR17 siRNA attenuates cerebral ischemic injury and inhibits the expression of inflammatory mediators in ischemic area.
赵冰
神经病学、精神病学基础医学医学研究方法
GPR17,脑缺血,大鼠,TNF-α,iNOs
GPR17 cerebral ischemia rats TNF-α,iNOs
赵冰.G蛋白偶联受体17对脑缺血损伤大鼠iNOs、TNF-α表达的影响[EB/OL].(2017-05-02)[2025-05-13].http://www.paper.edu.cn/releasepaper/content/201705-76.点此复制
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