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目的:探讨肿瘤坏死因子相关凋亡诱导配体(TNF-related apoptosis inducing ligand,TRAIL)及其受体——死亡受体4(death receptor 4,DR4)、诱骗受体1(decoy receptor 1,DcR1)在PCOS大鼠卵泡发育中的作用。方法:采用硫酸普拉睾酮钠诱导大鼠PCOS模型,免疫组织化学染色、RT-PCR分析观察TRAIL及其受体DR4、DcR1在PCOS大鼠卵巢颗粒细胞的表达情况。结果:①免疫组织化学结果显示,TRAIL蛋白在PCOS组大鼠卵巢窦状卵泡颗粒细胞的表达较对照组明显增强(P<0.05),在窦前卵泡颗粒细胞的表达两组无显著性差异(P>0.05)。DR4蛋白在两组大鼠窦前卵泡和窦状卵泡的表达无显著性差异(P>0.05)。DcR1蛋白在PCOS组大鼠卵巢窦状卵泡颗粒细胞的表达较对照组明显减弱(P<0.01),在窦前卵泡颗粒细胞的表达两组无显著性差异(P>0.05)。②RT-PCR分析显示,PCOS组大鼠卵巢颗粒细胞TRAIL mRNA的表达较对照组明显增强(P>0.01),DR4mRNA的表达两组无显著性差异(P>0.05),DcR1 mRNA的表达较对照组明显减弱(P<0.01)。结论:TRAIL及其受体DR4、DcR1在PCOS大鼠卵泡发育颗粒细胞凋亡中发挥了调控作用。TRAIL及其受体DR4、DcR1在PCOS颗粒细胞的表达异常可能是导致PCOS卵泡发育障碍的机制之一。
Objective: To investigate the effect of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) and its receptor-death receptor 4 (DR4), decoy receptor 1 (DcR1 ) In follicular development in PCOS rats. Methods: PCOS rat models were induced by sodium pramipexate sulfate. Immunohistochemical staining and RT-PCR were used to observe the expression of TRAIL and its receptors DR4 and DcR1 in ovarian granulosa cells of PCOS rats. Results ① Immunohistochemistry showed that the expression of TRAIL protein in granulosa cells of ovarian sinusoid in PCOS group was significantly higher than that in control group (P <0.05), but there was no significant difference between the two groups P> 0.05). There was no significant difference in the expression of DR4 between preantral follicles and sinusoid follicles in both groups (P> 0.05). The expression of DcR1 in ovarian sinusoidal granulosa cells in PCOS group was significantly lower than that in control group (P <0.01). There was no significant difference in the expression of DcR1 between the two groups (P> 0.05). (2) RT-PCR analysis showed that the expression of TRAIL mRNA in ovarian granulosa cells of PCOS group was significantly higher than that of the control group (P> 0.01), the expression of DR4 mRNA was not significantly different between the two groups (P> 0.05) Significantly weakened (P <0.01). Conclusion: TRAIL and its receptors DR4 and DcR1 play a regulatory role in the apoptosis of granulosa cells in PCOS rats. Abnormal expression of TRAIL and its receptors DR4 and DcR1 in PCOS granulosa cells may be one of the mechanisms that lead to follicular dysgenesis in PCOS.