【摘要】 目的从分子水平探讨PCOS患者发生胰岛素抵抗(IR)的分子生物学机制,研究多囊卵巢综合征PCOS脂肪组织肿瘤坏死因子受体II(TNFR2)mRNA的表达。方法采用RT-PCR技术结合内对(TNFR2)mRNA照,半定量检测PCOS及其对照组脂肪组织TNFR2mRNA的表达。结果TNFR2mRNA的表达在PCOS肥胖组(0.83±0.13,P<0.001〉)和PCOS非肥胖组(0.63±0.14,P<0.05)均显著大于非肥胖对照组(0.50±0.15),且以P-COS肥胖组升高更为明显(P<0.001),PCOS肥胖组与肥胖对照组(0.87±0.11)相比则无显著性(P>0.05)。结论高水平的肿瘤坏死因子a(TNFa)可通过上调TNFR2促进PCOS者TNFa系统活性增强。PCOS两组肥胖组织TNFR2mRNA的表达均较非肥胖对照组增强,且PCOS肥胖组升高更为显著。更多还原

【Abstract】 Objective To study the expression of TNFR2mRNA in adipose tissue from PCOS to get insight into the molecular mechanism of IR in PCOS.Methods The expression of TNFR2mRNA in adipose tissue was detected by semi-quantitative RT-PCR with inner-control.Results The expression of TNFR2mRNA in adipose tissue from the obese PCOS group(0.83±(0.13),P<0.001)and the nonobese PCOS group(0.63±0.14,P<0.05)was markedly higher than that in the nonobese control group(0.50±0.15),and the obese PCOS group presented a more increase(P<0.001).The difference between the obese PCOS group and the obese control group((0.87)±0.11)was no statistical significance(P>0.05).Conclusion These results suggest that the expression of TNFR2mRNA in adipose tissue from PCOS patient is abnormally excessive.The high TNFα could up-regulate TNFR2 which amplified the activity of TNFα in PCOS women.更多还原