冠心病痰瘀证型的胰岛素抵抗与单核细胞PPARγ mRNA表达

作者	单位
刘艳	浙江中医药大学附属第一临床医学院浙江省中医院
王坤根	浙江中医药大学附属第一临床医学院浙江省中医院
叶武	浙江中医药大学附属第一临床医学院浙江省中医院
陈杰	浙江中医药大学
陈隽妍	浙江中医药大学
华军益	浙江中医药大学
蔡宏文	浙江中医药大学附属第一临床医学院浙江省中医院
毛威	浙江中医药大学附属第一临床医学院浙江省中医院
许志良	浙江中医药大学附属第一临床医学院浙江省中医院

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中文摘要:

目的探讨冠心病(胸痹)痰瘀证型与胰岛素抵抗及外周血单核细胞过氧化物酶体增殖物激活受体γ信使核糖核酸(peroxisome proliferator activated receptor-γmessenger ribonucleic acid,PPARγmRNA)表达的关系。方法入选60例冠心病患者分为非痰非瘀组、痰凝心脉组及痰瘀互结组,每组各20例,另选健康志愿者20名为正常对照,测空腹血糖(FPG)、空腹胰岛素(FINS),计算胰岛素抵抗指数(homeostasis model assessment of insulin resistance,HOMA-IR),分离外周血单核细胞,应用逆转录-聚合酶链反应法(RT-PCR)检测PPARγmRNA的表达。结果与正常对照组比较,3个证型组患者FINS、HOMA-IR及PPARγmRNA表达水平均增高(P<0.01或P<0.05);与非痰非瘀组比较,痰凝心脉组及痰瘀互结组患者FINS、HOMA-IR和PPARγmRNA表达水平逐渐增高(P<0.05或P<0.01),且痰凝心脉组与痰瘀互结组的差异有统计学意义(P<0.05)。结论胰岛素抵抗和单核细胞PPARγmRNA的表达变化可能是冠心病(胸痹)痰瘀演变的机制之一。

英文摘要:

Objective To explore the relation of phlegm-stasis syndrome with insulin resistance and monocyte peroxisome proliferator activated receptor-γ messenger ribonucleic acid(PPARγ mRNA) expression in patients with coronary heart disease(CHD).Methods Sixty patients with CHD were differentiated into three syndrome types,the non-phlegm non-stasis(NN) type,the phlegm congealing heart vessel(PC) type and the phlegm-stasis cemented(PS) type.Besides,20 healthy volunteers were selected as the normal control.Levels of fasting plasma glucose(FPG) and fasting insulin(FINS) were determined and homeostasis model assessment of insulin resistance(HOMA-IR) was calculated accordingly.The expression of PPARγ mRNA in the peripheral monocytes was assessed by reverse transcriptase-polymerase chain reaction(RT-PCR).Results Levels of FINS,HOMA-IR and PPARγ mRNA expression in all CHD patients were higher than in the normal control(P<0.01,P<0.05);comparisons of the three indexes between patients of different syndrome types showed that they were higher in PC type and PS type than in NN type(P<0.05 or P<0.01),and the difference between PC type and PS type was significant(P<0.05).Conclusion Changes of insulin resistance and PPARγ mRNA expression in monocytes are possibly one of the mechanisms for the development of phlegm-stasis syndrome in CHD.

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