分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Herbal formula BaWeiBaiDuSan alleviates polymicrobial sepsis-induced liver injury via increasing the gut microbiota Lactobacillus johnsonii and regulating macrophage anti-inflammatory activity in mice

Xiaoqing Fan, Chutian Mai, Ling Zuo, Jumin Huang, Chun Xie, Zebo Jiang, Runze Li, Xiaojun Yao, Xingxing Fan, Qibiao Wu, Peiyu Yan, Liang Liu, Jianxin Chen, Ying Xie, Elaine Lai-Han Leung

Journal:Acta Pharmaceutica Sinica B

IF:14.9

DOI:10.1016/j.apsb.2022.10.016

PMID:36970196

Published:2022-10-22

research field:线粒体生理学低温生物学细胞生物学生殖生物学

Abstract

Sepsis-induced liver injury (SILI) is an important cause of septicemia deaths. BaWeiBaiDuSan (BWBDS) was extracted from a formula of Panax ginseng C. A. Meyer , Lilium brownie F. E. Brown ex Miellez var. viridulum Baker , Polygonatum sibiricum Delar. ex Redoute , Lonicera japonica Thunb., Hippophae rhamnoides Linn., Amygdalus Communis Vas, Platycodon grandiflorus (Jacq.) A. DC., and Cortex Phelloderdri . Herein, we investigated whether the BWBDS treatment could reverse SILI by the mechanism of modulating gut microbiota. BWBDS protected mice against SILI, which was associated with promoting macrophage anti-inflammatory activity and enhancing intestinal integrity. BWBDS selectively promoted the growth of Lactobacillus johnsonii (L. johnsonii) in cecal ligation and puncture treated mice. Fecal microbiota transplantation treatment indicated that gut bacteria correlated with sepsis and was required for BWBDS anti-sepsis effects. Notably, L. johnsonii significantly reduced SILI by promoting macrophage anti-inflammatory activity, increasing interleukin-10 + M2 macrophage production and enhancing intestinal integrity. Furthermore, heat inactivation L. johnsonii (HI- L. johnsonii ) treatment promoted macrophage anti-inflammatory activity and alleviated SILI. Our findings revealed BWBDS and gut microbiota L. johnsonii as novel prebiotic and probiotic that may be used to treat SILI. The potential underlying mechanism was at least in part, via L. johnsonii -dependent immune regulation and interleukin-10 + M2 macrophage production.

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