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作 者:刘鹏[1] 李晓青[1] 种莉[1] 唐鹏[1] 刘玥[1] 陈丽[1] 张欣[1] 侯辰[1] 李锐[1] 郭民侠[1]
出 处:《脑与神经疾病杂志》2014年第5期367-370,共4页Journal of Brain and Nervous Diseases
基 金:陕西省重点领域科技创新团队项目(2012KCT-17)
摘 要:目的观察氨中毒对体外大鼠培养神经元GABAA受体亚单位mRNA表达的影响,探讨肝性脑病(HE)发病机制。方法采用原位杂交技术,观察氨对体外培养新生大鼠神经元GABAA受体亚单位α1、β1及γ2mRNA表达的改变。结果与对照组相比,氨中毒神经元GABAA受体亚单位α1(增幅18%,P<0.05)、γ2(增幅23%,P<0.01)的mRNA表达显著上升,亚单位β1的mRNA表达无明显改变。结论氨可通过影响GABAA受体亚单位的表达发挥其对肝性脑病的致病作用。Objective To observe the expression of GABAA receptor subunits mRNA in vitro cultured rat neurons by ammonia intoxication,discuss the pathogenesis of hepatic encephalopathy (HE).Methods Using the hybridization in situ technique to observe the change of GABAA receptor subunits α1,β1 and γ2 mRNA in vitro cultured rat neurons by ammonia.Results In group of cultured neurons by ammonia,the expression levels of mRNA of GABAA receptor subunits α1 were increased amplitude 18% (P<0.05),γ2 increased amplitude 23% (P<0.01).Those increased significantly than those of control group.But subunitβ1 had no significant change in two groups.Conclusion The effect of ammonia on the HE could be conducted by modulating the expression of the GABAA receptor subunits.
分 类 号:R741[医药卫生—神经病学与精神病学]
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