YiMu-QingGong san alleviates lipopolysaccharide-induced endometritis in mice via inhibiting inflammation and oxidative stress through regulating macrophage polarization

文献类型： 外文期刊

第一作者： Yu, Yaming

作者： Yu, Yaming;Mao, Ningning;Yu, Lin;Lin, Fangzhu;Shi, Xiaofeng;Lu, Xuanqi;Yang, Yang;Wang, Deyun;Yu, Yaming;Mao, Ningning;Yu, Lin;Lin, Fangzhu;Shi, Xiaofeng;Lu, Xuanqi;Yang, Yang;Wang, Deyun;Lu, Yu

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关键词： Macrophage polarization; Inflammation; Endometritis; NF-kappa B; Fibrosis; Uterine barrier

期刊名称：JOURNAL OF ETHNOPHARMACOLOGY （ 影响因子：5.4； 五年影响因子：5.4 ）

ISSN： 0378-8741

年卷期： 2025 年 337 卷

页码：

收录情况： SCI

摘要： Ethnopharmacological relevance: Endometritis is a common reproductive disease in dairy cattle after calving, characterized by persistent inflammation of the endometrium. YiMu-QingGong San (YMQGS), a patented Chinese medicine formulation, has demonstrated efficacy in the treatment of clinical endometritis in dairy cattle. However, the potential mechanisms by which YMQGS alleviates endometritis remain unclear. Aim of the study: The objective of this study is to elucidate the underlying therapeutic mechanisms of YMQGS in the context of endometritis. Materials and methods: The chemical components of YMQGS were analyzed using UHPLC/MS. The antiinflammatory capabilities of YMQGS were assessed by inducing an inflammatory response in RAW264.7 cells with lipopolysaccharide (LPS). Moreover, a clinical model of endometritis was simulated via vaginal injection of LPS into the uterine horns to investigate the therapeutic mechanisms of YMQGS. Results: YMQGS could downregulate the expression of inflammatory mediators (TNF-alpha, IL-6, IL-1 beta) by suppressing the activation of the TLRs/MyD88/TRAF6/NF-kappa B signaling pathway in RAW264.7 cells. Additionally, YMQGS facilitated the polarization of RAW264.7 cells towards M2-like macrophages (M phi s) while inhibiting M1like M phi s polarization, thereby exerting anti-inflammatory effects. Further investigation revealed that YMQGS could diminish ROS production, augment cellular antioxidant capacity, preserve mitochondrial membrane potential, and reduce intracellular [Ca2+]i accumulation, thereby minimizing cellular damage. In the mouse model of endometritis, YMQGS similarly inhibited the activation of the NF-kappa B signaling pathway in uterine tissues and modulated M phi polarization in the endometrium, leading to a decrease in the expression of inflammatory factors and subsidence of the inflammatory response in the endometrium. Histological staining results showed that YMQGS reduced endometrial fibrosis, increased the expression of endometrial ZO-1, Occludin and glycoprotein, protect the endometrial barrier function, and prevent the further development of endometritis. Conclusion: Collectively, the present study confirms that YMQGS possesses notable anti-inflammatory and antioxidant properties. The suppression of the NF-kappa B signaling pathway and the modulation of M phi polarization emerge as the pivotal mechanisms by which YMQGS alleviates endometritis.

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