金雀异黄素对D-半乳糖损伤的乳鼠皮肤成纤维细胞的作用  

Study of genistein on mouse skin fibroblasts injured by D-galactose

作　　者：顾翠英[1] 韩志芬[1] 夏花英[1] 蒋嘉烨[1] 曹红平[1] 金国琴[1] 

机构地区：[1]上海中医药大学,上海201203

出　　处：《中国老年学杂志》2012年第24期5461-5464,共4页Chinese Journal of Gerontology

基　　金：上海市教育委员会重点学科建设资助项目(J50301);上海中医药大学校级资助项目(X196)

摘　　要：目的观察金雀异黄素(Gen)对D-半乳糖(D-gal)损伤的小鼠皮肤成纤维细胞(MSFs)模型的作用,并探索其机制。方法体外培养MSFs,D-gal制作细胞损伤模型,并用Gen进行干预。显微镜下观察各组MSFs生长形态变化;试剂盒法检测MSFs上清液中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和乳酸脱氢酶(LDH)活性;RT-PCR法检测MSFs的雌激素受体雌激素受体(ER)α和ERβmRNA的表达。结果与模型组相比,浓度为0.5 mg/L Gen能显著提高SOD活性,同时亦提高MDA含量和LDH活性(P<0.01);明显下调ERαmRNA表达(P<0.05),上调ERβmRNA表达(P<0.05)。结论浓度为0.5 mg/L Gen可以通过改善模型细胞ER mRNA的表达,提高SOD活性和抗氧化作用;同时升高MDA含量和LDH活性,改变MSFs的生物学特性,抑制其过度增殖。Objective To observe the effects of genistein （Gen） on the mouse skin fibroblasts （MSFs） injured by D-galactose and investigate the mechanisms. Methods MSFs were cultured in vitro, then Gen was used to affect the model cells injured by D-galactose. The morphostructure of the MSFs were observed with microscope. The vitalities of superoxide dismutase （ SOD ）, lactic acid dehydrogenase （LDH）, and the content of malondialdehyde （MDA） were measured by kit methods. ERotand ER[3mRNA were detected by RT-PCR method. Results Compared with model group, 0. 5 mg/L Gen could improve the content of MDA, increase the vitalities of SOD and LDH （P 〈 0. 01 ） markedly. Gen could decrease the expression of ERa mRNA （ P 〈 0. 05 ） and increase ERβ mRNA （ P 〈 0. 05） obviously. Couclusious 0. 5 mg/L Gen can improve ER mRNA, enhance the vitality of SOD and antioxidation, increase the content of MDA and the vitality of LDH, change the biological characteristics of MSFs, inhibit MSFs proliferation.

关 键 词：金雀异黄素 D-半乳糖 皮肤成纤维细胞 

分 类 号：R285.5[医药卫生—中药学]