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作 者:王霁雪[1] 王淑梅[1] 刘海岩[2] 付琳娜[3] 郑雅娟[1]
机构地区:[1]吉林大学第二医院,长春130041 [2]吉林大学基础医学院解剖教研室,长春130021 [3]长春生物制品研究所疫苗一室,长春130062
出 处:《中国生物制品学杂志》2010年第3期274-276,共3页Chinese Journal of Biologicals
基 金:国家自然科学基金资助课题(30571993)
摘 要:目的分析电压门控性氯通道ClC家族中的ClC-2氯通道在大鼠小梁网中的表达,探讨ClC-2在青光眼发病机制中的可能作用。方法经前房内注射玻璃酸钠建立大鼠慢性高眼压模型,取正常大鼠及模型大鼠小梁网组织,采用RT-PCR法检测ClC-2基因mRNA的转录水平,免疫组化法检测ClC-2蛋白的表达水平。结果在正常大鼠和慢性高眼压模型大鼠小梁网组织中,均可检测到ClC-2的表达,且模型大鼠ClC-2基因mRNA的转录水平和蛋白的表达水平均较正常大鼠降低。结论大鼠小梁组织中存在ClC-2氯通道的表达,该通道的表达受小梁网的一些病理因素的影响。Objective To investigate the expression of ClC-2 chloride channels in rat trabecular meshwork as well as possible role of ClC-2 in onset mechanism of glaucoma.Methods Rat model of chronic high intraocular pressure was established by injecting sodium hyaluronate into anterior chamber.The trabecular meshwork tissues of normal and model rats were isolated,in which the transcription level of ClC-2 mRNA was determined by RT-PCR,and the expression level of ClC-2 protein by immunohistochemical method.Results The transcription of ClC-2 mRNA and expression of ClC-2 protein were observed in the trabecular meshwork tissues of both normal and model rats,while the transcription and expression levels in model rats were lower than those in normal rats.Conclusion The expression of ClC-2 chloride channels was proved in rat trabecular meshwork,which was influenced by some pathological factors of trabecular meshwork.
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