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机构地区:[1]浙江中医药大学基础医学院病理生理教研室,浙江杭州310053
出 处:《浙江医学》2009年第9期1205-1207,共3页Zhejiang Medical Journal
基 金:浙江省自然科学基金资助项目(M303727).
摘 要:目的观察罗格列酮对氧化低密度脂蛋白(ox-LDL)诱导的肾小球系膜细胞(RMC)增殖和细胞外基质(ECM)分泌的影响。方法采用RT-PCR法检测正常对照组、ox-LDL组、罗格列酮组、罗格列酮+ox-LDL组RMC内的转化生长因子β1(TGFβ1)mRNA表达;同时采用MTT法检测各组RMC增殖水平,并予ELISA技术检测上清液中TGFβ1、层粘连蛋白(FN)、Ⅳ型胶原(ColⅣ)蛋白的含量。结果罗格列酮+ox-LDL组RMC增殖水平较ox-LDL组降低,且RMC表达的TGFβ1 mRNA水平和分泌的TGFβ1、FN、ColⅣ蛋白水平均较ox-LDL组降低(均P〈0.05或0.01)。结论罗格列酮可通过抑制ox-LDL诱导的RMC增殖和ECM及TGFβ1的分泌,从而发挥抗肾纤维化作用。Objective To investigate the effect of rosiglitazone on the proliferation of rat renal mesangial cells (RMCs) and synthesis of extracellular matrix induced by ox-LDL. Methods TGF- β1 mRNA expression of RMC in control group, ox-LDL group, rosiglitazone group and rosiglitazone+ox-LDL group were measured by RT-PCR. The cell proliferation was measured by MTT method. Synthesis of TGFβ1,FN,Col Ⅳ in cultured mesangial cells were determined by ELISA methods. Results In rosiglitazone+ox-LDL group, RMC proliferation was lower, compared with ox-LDL group. The TGFβ1 mRNA and protein levels of TGFβ1, FN, Col Ⅳ in rosiglitazone+ox-LDL group were also Rosiglitazone inhibited RMC proliferation, secretion of TGFβ1 antisirrhosis effect. ower than those in ox-LDL group (P〈0.05 or 0.01). Conclusion and extracelluar matrix, which may be associated with its antisirrhosis effect.
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