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作 者:李慧[1,2,3] 蔡霞[1] 桑春艳[3] 惠玲[2] 周杰[1] LI Hui;CAI Xia;SANG Chun-yan;HUI Ling;ZHOU Jie(Department of Neurosurgery Lanzhou General Hospital of Lanzhou Military Area Command,Lanzhou 730050,China;Medical Experiment Center Key Lab of Stem Cells and Genetaceutical of Gansu Province,1.Lanzhou General Hospital of Lanzhou Military Area Command,Lanzhou 730050,China;Lanzhou University,Lanzhou 730000,China)
机构地区:[1]兰州军区兰州总医院神经外科,兰州730050 [2]兰州军区兰州总医院医学实验中心甘肃省干细胞与基因药物重点实验室 [3]兰州大学,兰州730000
出 处:《解放军医药杂志》2018年第4期5-8,共4页Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
基 金:国家自然科学基金(81372177);甘肃省自然科学基金(1506RJZA301);军区医药卫生科研项目(CLZ14JB05)
摘 要:目的研究PPARγ基因对大鼠神经星形胶质细胞周期的影响及其分子机制。方法采用脂质体法将特异性针对过氧化物酶增殖物激活受体(PPARγ)基因的siRNA和阴性对照siRNA转至星形胶质细胞中,在常氧和低氧条件下分别培养48 h。蛋白免疫印迹试验分析PPARγ、CyclinD1、ERK、P-ERK蛋白表达情况;流式细胞仪检测细胞周期。结果成功将特异性的PPARγ siRNA脂质体转染到星形胶质细胞。与常氧条件比较,低氧条件下2组大鼠神经星形胶质细胞PPARγ、CyclinD1、ERK、P-ERK蛋白的表达及细胞增殖水平均明显升高(P<0.05)。siPPARγ组低氧和常氧条件下,大鼠神经星形胶质细胞中PPARγ、CyclinD1、P-ERK蛋白及低氧条件下ERK蛋白的表达及细胞增殖水平均低于阴性对照组(P<0.05)。结论 PPARγ基因参与了低氧条件下大鼠神经星形胶质细胞增殖的调控,其调节可能是通过ERK信号通路介导完成的。Objective To investigate effect and its mechanism of PPARγgene on nerval astrocyte cycle in rats.Methods Liposomes method was used for siRNA targeted to astrocytes in special directing peroxisome proliferator-activated receptorγ(PPARγ)gene(siPPARγgroup)and negative control group,and the transfected astrocytes were respectively cultured in normoxia and hypoxia for 48 h.Expressions of PPARγ,CyclinD1,ERK and P-ERK proteins were analyzed by western blotting method,and flow cytometer was used to detect cell cycle of astrocytes.Results Special PPARγsiRNA liposomes were transfected to astrocytes successfully.Compared with those under normoxia condition,PPARγ,CyclinD1,ERK and P-ERK protein expressions and cell proliferation levels in rats'nerval astrocytes were significantly increased under hypoxic condition in two groups(P<0.05).Under hypoxic and normoxic conditions,PPARγ,CyclinD1 and P-ERK protein expressions and ERK expression under hypoxic condition and cell proliferation levels in rats'nerval astrocytes in siPPARγgroup were significantly decreased compared with those in negative control group(P<0.05).Conclusion PPARγgene might be involved in proliferation regulation of rats'nerval astrocytes under hypoxic condition by regulating ERK pathway mediate.
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