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新型P2Y样G蛋白偶联受体GPR17在脑缺血损伤中的作用
目的 探讨新型P2Y样G蛋白偶联受体GPR17对脑缺血及缺氧缺糖(OGD)诱导皮层混合培养细胞中神经元损伤及小胶质细胞激活的影响.方法 ①以线栓法制备大鼠局灶性脑缺血模型,采用免疫组织化学、Western blottin...
赵冰魏尔清赵春贞张霞燕黄雪琴史文珍方三华卢韵碧张纬萍夏强
Aquaporin-4 deficiency attenuates acute lesions but aggravates delayed lesions and microgliosis after cryoinjury to mouse brain被引量:6
2012年
Objective To determine whether aquaporin-4 (AQP4) regulates acute lesions, delayed lesions, and the associated microglial activation after cryoinjury to the brain. Methods Brain cryoinjury was applied to AQP4 knockout (KO) and wild-type mice. At 24 h and on days 7 and 14 after cryoinjury, lesion volume, neuronal loss, and densities of microglia and astrocytes were determined, and their changes were compared between AQP4 KO and wild-type mice. Results Lesion volume and neuronal loss in AQP4 KO mice were milder at 24 h following cryoinjury, but worsened on days 7 and 14, compared to those in wild-type mice. Besides, microglial density increased more, and astrocyte proliferation and glial scar formation were attenuated on days 7 and 14 in AQP4 KO mice. Conclusion AQP4 deficiency ameliorates acute lesions, but worsens delayed lesions, perhaps due to the microgliosis in the late phase.
Wen-Zhen Shi Chun-Zhen Zhao Bing Zhao Xiao-Liang Zheng San-Hua Fang Yun-Bi Lu Wei-Ping Zhang Zhong Chen Er-Qing Wei
关键词:AQUAPORIN-4CRYOINJURYASTROCYTE
P2Y样G蛋白偶联受体GPR17参与缺糖缺氧诱导BV2小胶质细胞激活
目的 探讨P2Y样G蛋白偶联受体GPR17是否参与缺糖缺氧/恢复(OGD/R)诱导BV2小胶质细胞的激活。方法 以OGD诱导BV2小胶质细胞激活,以MTT 还原法检测细胞活性,以Western blotting和免疫细胞...
张壮黄静赵冰张霞燕方三华张纬萍魏尔清卢韵碧
半胱氨酰白三烯受体2通过介导小胶质细胞激活诱导缺血性神经元损伤
目的 探索半胱氨酰白三烯(CysLT)受体在大鼠皮层神经元缺氧缺糖损伤中的调节作用及作用机制.方法 培养大鼠原代皮层神经元或大鼠原代皮层混合培养细胞,以缺糖缺氧(OGD)模拟脑缺血损伤,以MTF还原法/LDH释放检测确定...
张霞燕黄雪琴赵春贞赵冰方三华卢韵碧张纬萍魏尔清
Aggravated inflammation and increased expression of cysteinyl leuko-triene receptors in the brain after focal cerebral ischemia in AQP4-deficient mice被引量:5
2012年
Objective Aquaporin-4 (AQP4), the main water channel protein in the brain, plays a critical role in water homeostasis and brain edema. Here, we investigated its role in the inflammatory responses after focal cerebral ischemia. Methods In AQP4-knockout (KO) and wild-type mice, focal cerebral ischemia was induced by 30 rain of middle cerebral arterial occlusion (MCAO). Ischemic neuronal injury and cellular inflammatory responses, as well as the expression and localization of cysteinyl leukotriene CysLT2 and CysLT~ receptors, were determined at 24 and 72 h after MCAO. Results AQP4-KO mice showed more neuronal loss, more severe microglial activation and neutrophil infiltration, but less astrocyte proliferation in the brain after MCAO than wild-type mice. In addition, the protein levels of both CysLT1 and CysLT2 receptors were up-regulated in the ischemic brain, and the up-regulation was more pronounced in AQP4-KO mice. The CysLT1 and CysLT2 receptors were primarily localized in neurons, microglia and neutrophils; those localized in microglia and neutrophils were enhanced in AQP4-KO mice. Conclusion AQP4 may play an inhibitory role in postischemic inflammation.
Wen-Zhen ShiChun-Zhen ZhaoBing ZhaoQiao-Juan ShiLi-Hui ZhangYan-Fang WangSan-Hua FangYun-Bi LuWei-Ping ZhangEr-Qing Wei
关键词:INFLAMMATIONMICROGLIAASTROCYTE
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