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一种网络药理学方法证实,鳖甲消症丸通过调节巨噬细胞炎症和肝星状细胞激活来对抗肝纤维化。

A network pharmacology approach confirms Biejiaxiaozheng pills combat hepatic fibrosis by modulating macrophage inflammation and hepatic stellate cell activation.

作者信息

Wu Weibin, Liao Yanli, Liang Jiefei, Huang Mi, Zhang Guifeng, Hu Yuying, Yuan Chao, Li Duanzhou

机构信息

School of Basic Medicine, Zhaoqing Medical College, Zhaoqing, Guangdong, China.

School of Public Health, Zhaoqing Medical College, Zhaoqing, Guangdong, China.

出版信息

Sci Rep. 2025 Jul 9;15(1):24638. doi: 10.1038/s41598-025-09002-1.

Abstract

Biejiaxiaozheng (BJXZ) pills, a traditional Chinese medicine, have demonstrated anti-fibrotic effects; however, their mechanisms in treating liver fibrosis remain unclear. This study aimed to explore the active targets and underlying mechanisms of BJXZ pills using network pharmacology and experimental validation. Network pharmacology analysis identified 213 common drug-disease targets, 1131 Gene Ontology terms, and 163 signaling pathways (including the TNF pathway). Experimental results showed that BJXZ pills significantly suppressed LPS-induced viability increase in RAW264.7 macrophages by inhibiting NF-κB activation (p-P65), reducing INOS expression, and decreasing inflammatory cytokines. They also alleviated oxidative stress by upregulating Nrf2 and HO-1, restoring mitochondrial membrane potential, and enhancing ATP production. Additionally, BJXZ pills markedly inhibited TGF-β-induced activation of LX-2 hepatic stellate cells, reducing fibrotic markers like α-SMA. These findings suggest that BJXZ pills exert anti-fibrotic effects via multiple pathways, with the TNF pathway playing a key role. Mechanistically, the protective effects involve suppressing macrophage and hepatic stellate cell activation, highlighting BJXZ pills as a promising therapeutic option for liver fibrosis.

摘要

鳖甲消症(BJXZ)丸是一种中药,已显示出抗纤维化作用;然而,其治疗肝纤维化的机制仍不清楚。本研究旨在利用网络药理学和实验验证来探索鳖甲消症丸的活性靶点和潜在机制。网络药理学分析确定了213个常见的药物 - 疾病靶点、1131个基因本体术语和163条信号通路(包括TNF通路)。实验结果表明,鳖甲消症丸通过抑制NF-κB激活(p-P65)、降低诱导型一氧化氮合酶(INOS)表达和减少炎性细胞因子,显著抑制脂多糖(LPS)诱导的RAW264.7巨噬细胞活力增加。它们还通过上调核因子E2相关因子2(Nrf2)和血红素加氧酶-1(HO-1)、恢复线粒体膜电位和增强ATP生成来减轻氧化应激。此外,鳖甲消症丸显著抑制转化生长因子-β(TGF-β)诱导的LX-2肝星状细胞激活,减少诸如α-平滑肌肌动蛋白(α-SMA)等纤维化标志物。这些发现表明,鳖甲消症丸通过多种途径发挥抗纤维化作用,其中TNF通路起关键作用。从机制上讲,其保护作用涉及抑制巨噬细胞和肝星状细胞激活,突出了鳖甲消症丸作为肝纤维化一种有前景的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff59/12241332/81b731339a18/41598_2025_9002_Fig1_HTML.jpg

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