月见草油对PCOS模型大鼠NLRP3炎症体通路的影响

    Effects of Evening Primrose Oil on NLRP3 Inflammatory Pathway in PCOS Model Rats

    • 摘要:
      目的 探讨月见草油(evening primrose oil,EPO)对多囊卵巢综合征(polycystic ovarian syndrome,PCOS)模型大鼠NLRP3炎症体通路的改善作用及机制。
      方法 6周龄SD大鼠,连续21 d灌胃来曲唑联合高脂饲料喂养,建立PCOS模型。成模后给予不同剂量的EPO,期间测体质量、空腹血糖(fasting plasma glucose,FPG)及动情周期等。取完材后用ELISA测定空腹胰岛素(fasting insulin,FINS)、促黄体生成素(luteinizing hormone,LH)等激素水平;TUNEL法检测大鼠卵巢颗粒细胞凋亡情况;HE染色法观察卵巢形态学变化;Western blotting和免疫组织化学染色法检测卵巢组织NLRP3、ASC、TNF-α、IL-18等蛋白。
      结果 与PCOS模型组比较,EPO干预后,PCOS大鼠体质量、FPG及LH等水平显著改善(P<0.05),卵巢多囊病变减轻,NLRP3、ASC、TNF-α、IL-18等炎症因子表达水平均明显降低,差异有统计学意义。
      结论 EPO可以改善PCOS大鼠卵巢组织形态,降低FPG以及血清中FINS、LH等激素水平,同时可能通过调控NLRP3炎症体通路改善PCOS慢性炎症。

       

      Abstract:
      OBJECTIVE  To investigate the effect and mechanism of evening primrose oil(EPO) on NLRP3 inflammatory pathway in polycystic ovarian syndrome(PCOS) model rats.
      METHODS  Six-week-old SD rats were fed with letrozole combined with high-fat diet for 21 days to establish PCOS model. After forming the model, different doses of EPO were given to measure body mass, fasting plasma glucose(FPG) and estrus cycle. The levels of fasting insulin(FINS), luteinizing hormone(LH) and other hormones were determined by ELISA. The apoptosis of ovarian granulosa cells was detected by TUNEL method. The morphological changes of ovary were observed by HE staining. Western blotting and immunohistochemical staining were used to detect NLRP3, ASC, TNF-α, IL-18 and other proteins in ovarian tissue.
      RESULTS  Compared with PCOS model group, after intervention with EPO, body weight, FPG and LH levels of PCOS rats were significantly improved(P<0.05), polycystic ovarian disease was alleviated, and the expression levels of NLRP3, ASC, TNF-α, IL-18 and other inflammatory factors were significantly decreased, with statistical significance.
      CONCLUSION  EPO can improve the ovarian tissue morphology of PCOS rats, reduce the levels of FPG, FINS, LH and other hormones in serum, and may improve the chronic inflammation of PCOS by regulating the NLRP3 inflammatory pathway.

       

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