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目的:研究来曲唑(LE)诱导的多囊卵巢综合征(PCOS)大鼠模型卵巢组织中脑源性神经营养因子(BDNF)及其受体——TrkB蛋白的表达及对卵泡发育的影响。方法:应用LE诱导大鼠PCOS模型,放射免疫法测定大鼠血清性激素水平,酶联免疫法(ELISA)测定血清细胞色素P450芳香化酶(P450arom)含量;HE染色观察卵巢组织学变化;免疫印迹法检测BDNF及其TrkB蛋白在卵巢组织中的表达;免疫组织化学法检测TrkB在各级卵泡中的表达差异。结果:与对照组比较,模型组血清睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)浓度显著增高,雌二醇(E2)、孕酮(P)浓度显著降低,血清P450arom含量显著降低;差异均有统计学意义(P<0.05)。模型组卵巢体积增大,囊状扩张卵泡明显增多,黄体数量明显减少。模型组卵巢组织中BDNF蛋白表达水平显著高于对照组(P<0.01),而TrkB在卵巢组织中的表达有2个片段,即fl-TrkB和tr-TrkB。fl-TrkB在模型组的表达明显高于对照组,而tr-TrkB的表达明显低于对照组,差异均有统计学意义(P<0.01)。TrkB在各级卵泡卵母细胞上的表达呈递减趋势;模型组大窦前卵泡的颗粒细胞中的表达强度高于对照组,在卵母细胞中的表达强度低于对照组(P<0.05);在模型组囊状卵泡颗粒细胞中的表达强度远高于对照组窦状卵泡颗粒细胞的表达,且差异有统计学意义(P<0.05)。结论:LE诱导的PCOS大鼠模型是研究PCOS病理机制的一种理想的动物模型,卵巢组织内BDNF/TrkB表达水平的变化可能与PCOS卵泡发育障碍相关。
AIM: To investigate the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB in ovarian tissue of leukemia-induced polycystic ovary syndrome (PCOS) rats and its effect on follicular development . Methods: Serum levels of sex hormones were determined by radioimmunoassay (RIA) in rats. Serum levels of cytochrome P450 (P450arom) were measured by enzyme-linked immunosorbent assay (ELISA). Histological changes were observed by HE staining. Method was used to detect the expression of BDNF and its TrkB protein in ovarian tissue. Immunohistochemical method was used to detect the expression of TrkB in all levels of follicles. Results: Compared with the control group, the concentrations of serum testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) in model group were significantly increased, while the concentrations of estradiol (E2) and progesterone Content was significantly lower; the differences were statistically significant (P <0.05). Ovarian volume of the model group increased, cystic dilatation follicles increased significantly, the number of corpus luteum decreased significantly. The expression of BDNF protein in the ovarian tissue of the model group was significantly higher than that of the control group (P <0.01), while the expression of TrkB in the ovary tissue was twofold, namely fl-TrkB and tr-TrkB. The expression of fl-TrkB in the model group was significantly higher than that in the control group, while the expression of tr-TrkB was significantly lower than that in the control group (P <0.01). The expression of TrkB in follicular oocytes showed a decreasing trend. The expression of granulosa cells in model group was higher than that in control group, and the expression level in oocytes was lower than that in control group (P <0.05) ; The expression intensity of cystic granulosa cells in the model group was much higher than that in the control group, and the difference was statistically significant (P <0.05). CONCLUSION: The PC-induced rat model of PCOS is an ideal animal model for the study of pathological mechanism of PCOS. The change of BDNF / TrkB expression in ovarian tissue may be related to follicular dysplasia in PCOS.