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Pioglitazone stimulates Na+/ H+ exchanger 1(NHE1) transfer by PPARγ/ ERK pathway in the mice embryonic fibroblast cells

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF DIABETES
Issue:
9
DOI:
10.3969/j.issn.1006-6187.2010.09.017
Key Word:
吡格列酮;过氧化物酶体增殖物活化受体;细胞外信号调节激酶;胚胎成纤维细胞;Na+/H+离子转运体

Abstract: 目的 研究吡格列酮对钠氢离子转运体(NHE1)的转运作用及传导通路,探讨噻唑烷二酮类药物引起水肿的机制. 方法 野生及PPARγ-/-鼠胚胎成纤维细胞分为:对照组(DMEM培养液),ERK抑制剂(10μmol/L PD98059)组,PPARγ拮抗剂(5μmol/L GW9662)组,基因转录抑制剂(5μmol/L Actiomycin D)组.测定各组细胞在0.3μmol/L吡格列酮灌注下NHE1的活性,Western blot法测定ERK磷酸化. 结果 吡格列酮增加野生鼠NHE1活性48.1%±3.1%,其作用被ERK抑制剂及PPARγ拮抗剂阻止,而不被基因转录抑制剂阻止;吡格列酮刺激野生鼠ERK磷酸化,对PPARγ-/- 鼠无此作用.结论吡格列酮经PPARγ/ERK通路,不依赖基因转录,刺激鼠胚胎成纤维细胞NHE1的转运,促进钠潴留.

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