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 postpartum uterine inflammation model in rats, and to investigate the internal mechanism of motherwort on postpartum uterine involution from the perspective of molecular biology. Methods Rats were randomly divided into four groups: control, model, motherwort, and Notoginseng groups. Uterine inflammation model was set up with Notoginseng as positive control, ELISA method was used to detect the serum tumor necrosis factor-α (TNF-α) levels in rats, rat uterus in various groups was observed by HE staining, and the expression of matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metallo- proteinase type I (TIMP-1), and collagen I in uterine tissue was detected by immunohistochemical method. Results Serum TNF-α levels in the model group were significantly higher than that in the control group; Compared with the model group, serum TNF-α levels in motherwort group decreased significantly. Compared with control group, MMP-13 and TIMP-1 were significantly increased in the model group, and expression of collagen I was up-regulated. Compared with the model group, MMP-13 in motherwort group had no significant change, and expression of TIMP-1 and collagen I was significantly reduced. Conclusion This experiment confirms that motherwort could possibly reduce TNF-α levels in rats with postpartum uterine inflammation and the expression of TIMP-1 to start the repair mechanism of stop bleeding, and accelerate the degradation of extracellular matrix (ECM), so as to speed up postpartum uterine involution.

国家自然科学基金项目资助（30572405）