摘要
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 metalloproteinase 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.
出处
《药物评价研究》
CAS
2012年第4期246-249,共4页
Drug Evaluation Research
基金
国家自然科学基金项目资助(30572405)