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前列腺素E1改善高糖联合肿瘤坏死因子-α损伤HBZY-1细胞及机制研究

来自:中国糖尿病杂志  编辑:袁园 薛耀明 江颖娟 张倩|点击数:|2013-12-25

  ·糖尿病基础研究·

  【摘要】 目的 观察前列腺素E1(PGE1)对高糖联合肿瘤坏死因子-α(TNF-α)诱导的大鼠肾小球系膜细胞株(HBZY-1)损伤的影响及机制。 方法 将HBZY-1细胞分为正糖(NG)组、高糖+TNF-α(HT)组、高糖+TNF-α+不同浓度PGE1(HTP1~HTP5)组,采用MTT法测定细胞增殖,ELISA与RT-PCR法测定细胞上清液中单核细胞趋化蛋白-1(MCP-1)、转化生长因子-β1(TGF-β1)以及白介素-6(IL-6)蛋白含量及mRNA表达,细胞免疫荧光法测定核因子-κB p65(NF-κB p65)核转位。 结果 高糖联合TNF-α促进HBZY-1增殖,增加MCP-1、TGF-β1蛋白与mRNA,以及IL-6mRNA的表达(P<0.05),同时促进NF-κB p65的核转位;1 ng/mLPGE1抑制以上作用(P<0.05)。 结论 PGE1通过抑制NF-κB通路来抑制高糖联合TNF-α诱导的HBZY-1增殖,降低MCP-1、TGF-β1,以及IL-6蛋白及基因表达。

  【关键词】前列腺素E1;大鼠系膜细胞;高糖;肿瘤坏死因子-α;核因子-κB

PGE1 ameliorates injury of rat mesangial cells induced by high glucose and TNF-α and its potential mechanism YUAN Yuan,XUE Yao-ming,JIANG Ying-juan,et al. Department of Endocrinology and Metabolism,Nanfang Hospital,Southern Medical University,Guangzhou 510515,China

Corresponding author :XUE Yao-ming,E-mail:xueyaoming999@126.com

  【Abstact】 Objective To investigate the effects of PGE1 on injury of rat mesangial cells(HBZY-1) induced by high glucose and TNF-α and its possoble mechanism. Methods Rat mesangial cells were cultured in the presence of high glucose and TNF-α with different concentrations of PGE1.Cell proliferation was tested by MTT .The protein level of MCP-1,TGF-β1 and IL-6 in cultural supernatants were measured by enzyme linked immunosorbent assay.The mRNA expressions of MCP-1,TGF-β1 and IL-6 were measured by real-time fluorescent quantitative PCR,and NF-κB p65 translocation was detected using immunofluorescence assay. Result High glucose combined with TNF-α obviously promoted HBZY-1 proliferation and increased the protein and mRNA expression of MCP-1 and TGF-β1, and IL-6 mRNA expression(P<0.05),and at the same time promoted nuclear transfer of NF-κB p65.And PGE1 inhibited above actions(P<0.05). Conclusion PGE1 can restrain HBZY-1 proliferation induced by high glucose and TNF-α , and reduce the expression of MCP-1, TGF-β1 and IL-6 protein and mRNA via NF-κB pathway.

  【Key word】 Prostaglandin E1( PGE1);Rat mesangial cell;High glucose;Tumor necrosis factor-α(TNF-α);Nuclear factor-κB(NF-κB)

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