摘要
目的观察过氧化物酶体增殖体激活受体-γ(PPAR-γ)激活对糖基化终末产物(AGEs)引起的大鼠肾系膜细胞TGF-β及CTGFmR-NA表达的影响。方法体外培养正常大鼠肾系膜细胞,逆转录聚合酶链式反应(RT-PCR)检测不同浓度AGEs(0～400μg/ml-1)及不同浓度PPAP-γ)激活剂(罗格列酮)和PPAR-γ阻断剂(GW9662)对AGEs(100μg/ml-1)引起的TGF-β及CTGFmRNA表达的影响。结果给予PPAR-γ激活剂可明显减轻AGEs引起的大鼠系膜细胞TGF-β、CTGFmRNA的表达。结论PPAR-γ激活剂可以明显减轻AGEs对系膜细胞TGF-β、CTGFmRNA的表达影响,从而改善肾小球细胞外基质积聚,在糖尿病时起到肾脏保护作用。
Objective To investigate the role of peroxisome proliferator-activated receptor（PPAR）-γ activation on the expressions of TGF-β and CTGF mRNA in rat mesangial cells extenuation induced by advanced glycation end products （AGEs）.Methods Rat mesangial cells were treated with AGE-modified bovine serum albumin or native bovine serum albumin.Normal mesangial cells without any treatments were as control.TGF-β and CTGF mRNA were analyzed by reverse transcriptase-polymerase chain reaction （RT-PCR）.The expressions of TGF-β and CTGF mRNA in mesangial cell induced by rosiglitazone （0～10 μmol/L） and the inhibitor of PPAR-γ（10 μmol/L） were tested with RT-PCR.Results PPAR-γ activation relieved TGF-β and CTGF mRNA expressing induced by AGEs（0～400 mg/L） in mesangial cells.Conclusions PPAR-γ activation can relieve the expressions of TGF-β and CTGF mRNA in rat mesangial cells induced by AGEs,suggesting that PPAR-γ activation has a kidney protection in diabetic mellitus through ameliorating extracellular matrix accumulation.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2010年第8期1062-1064,共3页
Chinese Journal of Gerontology
基金
国家自然科学基金资助课题(30800423)
