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机构地区:[1]华中科技大学同济医学院附属协和医院眼科,湖北武汉430022
出 处:《眼视光学杂志》2002年第2期92-94,共3页Chinese Journal of Optometry & Ophthalmology
基 金:国家自然科学基金资助项目 (3 8970 75 8)
摘 要:目的 :观察tranilast对转化生长因子 β2 (transform inggrowthfactor β2 ,TGF β2 )抑制体外培养人眼小梁细胞生长作用的影响。方法 :采用MTT法观察 0 μg/ml、12 .5 μg/ml、2 5μg/ml和 5 0 μg/mltranilast对 3.2ng/mlTGF β2 抑制体外培养人眼小梁细胞生长作用的影响。结果 :2 5 μg/ml和 5 0 μg/ml收稿日期 :2 0 0 2 -0 3 -2 7;修回日期 :2 0 0 2 -0 4-15基金项目 :国家自然科学基金资助项目 (3 8970 75 8)。作者简介 :曹阳 (1972 -) ,男 ,湖北武汉人 ,医学博士 ,主治医师 ,研究方向 :青光眼。通信作者 :曹阳 (E -mail:ytsao @sohu .com)。tranilast处理组人眼小梁细胞的光密度A值分别为 (1.136±0 .135 )和 (1.2 4 6± 0 .15 2 ) ,与对照组的 (0 .896± 0 .190 )比较 ,差异分别有显著性 (q =3.2 3,P <0 .0 5 )和非常显著性 (q =4 .70 ,P <0 .0 1)。结论 :Tranilast可明显拮抗TGF β2 对体外培养人眼小梁细胞抑制生长的作用。利用Tranilast在发病学环节防治原发性开角型青光眼的可能性 。Objective:To investigate the effect of tranilast on the inhibition of proliferation induced by TGF β 2 in cultured human trabecular meshwork cells.Methods:Human trabecular meshwork cells were cultured in vitro,then identified under the microscope using SEM and immunohistochemical stain. Suspension of 1×10 4 cultured human trabecular meshwork cells of 3~5 passage was distributed in each well of a 96 well disk and divided into a control group and an experimental group. After 24 hours,0 μg·ml -1 (control)?12.5 μg·ml -1 ?25 μg·ml -1 ?50 μg·ml -1 tranilast with 3.2 ng·ml -1 TGF β 2 were added into the incubation medium. After another 24 hours,the proliferation in cultured human trabecular meshwork cells was examined using a tetrazolium based semiautomated colormetric(MTT) assay.Results:Cultured cells had the specific characteristics of human trabecular meshwork cells. Absorbance values of the experimental group were 0.9036±0.3017,1.1361±0.1352,1.2457±0.1524,according to the different concentrations of tranilast,and 0.8956±0.1903 for the control group. In comparison to the control group,25 μg·ml -1 (q'=3.23,P<0.05),50 μg·ml -1 (q'=4.70,P<0.01) tranilast significantly antagonized the decrease of the absorb.Conclusion:Tranilast has an antagonistic effect on the inhibition of proliferation induced by TGF β 2 in the cultured human trabecular meshwork cells. Since the drugs currently in use for POAG therapy still only provide remedies by lowering intraocular pressure,the possible role of tranilast as a drug to treat the pathogenesis of POAG effectively is worth further investigation.
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