Objective:To establish a post-partum uterine inflammation model in rats, from the perspective of molecular biology of postpartum uterine involution motherwort internal mechanism.Methods:Rats were randomly divided into 4 groups:blank control group, model group, motherwort group Notoginseng group. Uterus inflammation model set up with three extracts-PNS for positive control, using ELISA method on the serum TNF-αand TGF-β1 levels were measured in rats of various organizations of the uterus for HE staining, and by immunohistochemical detection of uterine tissue MMP-2, MMP-13, TIMP-1, Collagen1, Fibronection expression.Results:Serum TNF-α, TGF-β1 levels were significantly higher than the control group; compared with the model group, serum motherwort TNF-α, TGF-β1 levels decreased significantly. The model group compared with control group, MMP-2, MMP-13, TIMP-1 was significantly increased, Collagen1, Fibronection expression, compared with the model group, motherwort group MMP-2, MMP-13 no significant change, TIMP-1, Collagen1, Fibronection expression significantly reduced. Conclusion:E. coli can be used to copy the success of post-partum endometrial inflammation model. This experiment confirmed that Motherwort is possible postpartum uterine inflammation TNF-α, TGF-β1 levels, reduced the expression of TIMP-1 to start the repair mechanism to stop bleeding and accelerate the degradation of ECM, in order to speed up post-partum uterine involution. |