Bushen Huoxue formula attenuates recurrent spontaneous abortion by modulating arginine metabolism and macrophage polarization at the maternal-fetal interface

IF 3.1 3区医学 Q2 CHEMISTRY, ANALYTICAL

Journal of pharmaceutical and biomedical analysis Pub Date : 2025-09-24 DOI:10.1016/j.jpba.2025.117161

Jingyi Song , Yuan Xu , Jihong Liu , Yuqing Zhong , Ying Hong , Shiqi Liu , Xiaojun Gou , Yan Wu , Quanfang Jin

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引用次数: 0

Abstract

The aim of this study was to clarify the effects of BSHXF on pregnancy outcome and macrophage polarization at the maternal-fetal interface in a mouse model of recurrent spontaneous abortion (RSA). The RSA model was established using the CBA/J × DBA/2 mating method. Network pharmacology predicted the mechanism of BSHXF intervention in RSA and verified by Western blotting. Immunofluorescence and RT-qPCR were used to measure the levels of macrophage-associated cytokines at the maternal-fetal interface. Placental metabolomics was used to analyze the mechanism of macrophage regulation by BSHXF and verified by ELISA. BSHXF improved embryonic resorption and hormone levels in RSA mice and restored abnormal NF-κB signaling, which was achieved in part by modulating macrophage polarisation status. BSHXF intervention decreased M1 macrophage polarization while elevating M2 macrophage levels. Metabolomics indicated that decreased inducible nitric oxide synthase (iNOS) pathway and elevated arginase-1 pathway (Arg-1) pathway in the placenta were the key mechanisms of macrophage polarization. This study provides innovative insights into the mechanism by which BSHXF ameliorates RSA in mice, providing a scientific basis for further pharmacological research.

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补肾活血方通过调节母胎界面的精氨酸代谢和巨噬细胞极化，减轻复发性自然流产。

本研究的目的是阐明BSHXF对复发性自然流产（RSA）小鼠模型妊娠结局和母胎界面巨噬细胞极化的影响。采用CBA/J × DBA/2匹配方法建立了RSA模型。网络药理学预测BSHXF干预RSA的机制，并通过Western blotting验证。采用免疫荧光和RT-qPCR检测母胎界面巨噬细胞相关细胞因子水平。采用胎盘代谢组学分析BSHXF调控巨噬细胞的机制，并通过ELISA进行验证。BSHXF改善了RSA小鼠的胚胎吸收和激素水平，并恢复了异常的NF-κB信号传导，部分是通过调节巨噬细胞极化状态实现的。BSHXF干预降低了M1巨噬细胞极化，同时提高了M2巨噬细胞水平。代谢组学表明，胎盘诱导型一氧化氮合酶（iNOS）通路的降低和精氨酸酶-1通路（Arg-1）通路的升高是巨噬细胞极化的关键机制。本研究为BSHXF改善小鼠RSA的机制提供了创新的见解，为进一步的药理研究提供了科学依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of pharmaceutical and biomedical analysis 医学-分析化学

CiteScore

6.70

自引率

5.90%

发文量

588

审稿时长

37 days

期刊介绍： This journal is an international medium directed towards the needs of academic, clinical, government and industrial analysis by publishing original research reports and critical reviews on pharmaceutical and biomedical analysis. It covers the interdisciplinary aspects of analysis in the pharmaceutical, biomedical and clinical sciences, including developments in analytical methodology, instrumentation, computation and interpretation. Submissions on novel applications focusing on drug purity and stability studies, pharmacokinetics, therapeutic monitoring, metabolic profiling; drug-related aspects of analytical biochemistry and forensic toxicology; quality assurance in the pharmaceutical industry are also welcome. Studies from areas of well established and poorly selective methods, such as UV-VIS spectrophotometry (including derivative and multi-wavelength measurements), basic electroanalytical (potentiometric, polarographic and voltammetric) methods, fluorimetry, flow-injection analysis, etc. are accepted for publication in exceptional cases only, if a unique and substantial advantage over presently known systems is demonstrated. The same applies to the assay of simple drug formulations by any kind of methods and the determination of drugs in biological samples based merely on spiked samples. Drug purity/stability studies should contain information on the structure elucidation of the impurities/degradants.