摘要
目的探讨地塞米松对永生化人眼小梁细胞的流畅阻力和水通道蛋白-1(AQP-1)表达的影响。方法将永生化人眼小梁细胞株第18代接种于0.4μm孔径的滤膜上,待细胞近融合时加入含10-7mol/L地塞米松培养液。细胞融合后1、3、7d,应用内皮细胞电阻测量仪(EVOM)测定滤膜上单层小梁细胞电阻(TEER),评价其流畅阻力的变化;采用免疫印迹法检测小梁细胞AQP-1的表达情况。结果细胞融合后1、3、7d时,对照组TEER分别为(36.4±1.4)Ω、(34.0±1.7)Ω、(36.1±2.9)Ω,而经地塞米松处理组TEER则分别为(48.4±2.3)Ω、(60.3±3.1)Ω、(58.8±0.9)Ω,差异有统计学意义。用免疫印迹法检测,显示经地塞米松处理后的小梁细胞AQP-1表达量较未经处理组增多,差异亦有统计学意义。结论经地塞米松处理后的滤膜上小梁细胞AQP-1表达水平上调、表达量增多,小梁细胞TEER也升高,提示地塞米松上调AQP-1的表达水平可能与小梁细胞的流畅阻力改变有关。应用EVOM检测TEER可以体现内壁单层小梁细胞的流畅阻力,将为房水引流的研究提供新手段。(中华眼科杂志,2005,41:209-211)
Objective To study the effect of dexamethasone on trans epithelial electrical resistance （TEER） and the expression of AQP-1 in immortalized trabecular ceils. Methods Immortalized human trabecular cells were cultured on PET membrane in 24 wells plate. The cells were treated with Dexamethasone in concentration of 10-7 mol/L. After the cultured cell became confluence, TEER of the cells was detected to evaluate the resistance of outflow pathway at different time points. Western blot was used to analyze the expression of AQP-1 in the trabecular cells. Results The TEER and the expression of AQP-1 were much higher in the cells treated by Dexamethasone in comparison to control without dexamethasone exposure. Conclusions The TEER and expression of AQP-1 in immortalized trabecular cells can be enhanced by Dexamethasone. AQP-1 upregulation induced by Glucocorticoid may relate with the increased resistance of outflow pathway in glaucoma.
出处
《中华眼科杂志》
CAS
CSCD
北大核心
2006年第3期209-211,共3页
Chinese Journal of Ophthalmology
基金
国家自然科学基金资助项目(30271386)
全国百优博士论文作者专项基金资助项目(200363)
广东省自然科学基金资(021823)
广东省科技计划资助项目(C30503)
关键词
小梁网
细胞生理学
水孔蛋白类
地塞米松
Trabecular meshwork
Cell physiology
Aquaporins
Dexamethasone
