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目的建立产后大鼠子宫炎症模型,从分子生物学角度探讨益母草对产后子宫复旧的内在机制。方法将大鼠随机分为4组:空白对照组、模型组、益母草组、三七总皂苷组。建立产后子宫炎症模型,用三七总皂苷作阳性对照,采用ELISA法对各组大鼠血清肿瘤坏死因子-α(TNF-α)的量进行测定,对各组大鼠的子宫组织进行HE染色观察,同时用免疫组化法检测子宫组织中基质金属蛋白酶-13(MMP-13)、金属蛋白酶组织抑制因子-1(TIMP-1)、I型胶原(collagen I)的表达。结果模型组血清TNF-α水平明显高于空白对照组;与模型组比较,益母草组血清TNF-α水平显著降低。模型组与空白对照组比较,MMP-13、TIMP-1明显升高,collagen I表达上调;与模型组比较,益母草组MMP-13无明显变化,TIMP-1明显降低,collagen I表达下降。结论益母草可能使产后炎症子宫的TNF-α水平下降,下调TIMP-1的表达,启动止血修复机制,并加快细胞外基质(ECM)降解,从而加速产后子宫复旧。
Objective To establish a model of uterine inflammation in postpartum rats and to explore the intrinsic mechanism of Leonurus on postnatal uterine involution from the perspective of molecular biology. Methods The rats were randomly divided into 4 groups: blank control group, model group, motherwort group, Panax notoginseng saponins group. The model of postpartum uterine inflammation was established, and the total RNA of Panax notoginseng was used as the positive control. The amount of tumor necrosis factor-α (TNF-α) in serum of each group was measured by ELISA. HE staining The expressions of MMP-13, TIMP-1 and collagen I in uterine tissue were detected by immunohistochemistry. Results The levels of serum TNF-α in the model group were significantly higher than those in the blank control group. Compared with the model group, serum TNF-α level was significantly lower in the motherwort group. The expression of MMP-13 and TIMP-1 in the model group was significantly higher than that in the blank control group, and the expression of collagen I was up-regulated. Compared with the model group, MMP-13 in the motherwort did not change significantly, TIMP-1 decreased and collagen I expression decreased. Conclusion Motherwort may reduce the level of TNF-α, decrease the expression of TIMP-1, activate the hemostatic repair mechanism and accelerate the degradation of extracellular matrix (ECM) in postpartum inflammatory womb, so as to accelerate the postpartum uterine involution.