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作 者:杨荫[1] 郑煜[1] 陈祁[1] 王乾成[1] 赵书[1] 陈丽[1]
机构地区:[1]四川大学华西基础医学与法医学院生理学教研室,四川成都610041
出 处:《西部医学》2011年第3期405-407,共3页Medical Journal of West China
基 金:国家自然科学基金(No.30370530)
摘 要:目的探讨慢性缺氧对大鼠岩神经节神经元酸敏感离子通道(acid-sensingion channels,ASICs)的两种亚型ASIC1a和ASIC1b表达的变化。方法建立大鼠慢性缺氧模型(6 h/d,12 d),用常规免疫组化法(PV法)观察正常大鼠及慢性缺氧大鼠岩神经节神经元ASIC1a和ASIC1b的表达。结果正常大鼠岩神经节存在ASIC1a和ASIC1b阳性表达神经元;慢性缺氧组大鼠岩神经节ASIC1a和ASIC1b阳性神经元明显多于正常组(P<0.05)。结论慢性缺氧能上调大鼠岩神经节神经元ASIC1a和ASIC1b的表达。Objective To investigate the effect of chronic hypoxia on expression of ASIC1a and ASIC1b of the neurons in petrosal ganglions of rats.Methods Sprage-Dawley rats were randomly divided into normal group and chronic hypoxia group.Chronic hypoxia models of rats were established(6h/day,12days).The protein expression levels of ASIC1a and ASIC1b were determined by immunohistochemical staining.Results ASIC1a and ASIC1b-positive immunoreactive neurons were observed in petrosal ganglions of normal rats.ASIC1a and ASIC1b-positive immunoreactive neurons were significantly increased in the rats with chronic hypoxia(P0.05).Conclusion The expression of ASIC1a and ASIC1b of the neurons in petrosal ganglions of rats can be up-regulated by chronic hypoxia.
分 类 号:R338.2[医药卫生—人体生理学] Q24[医药卫生—基础医学]
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