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五味子乙素通过调节小鼠的PPARγ信号通路和肠道微生物群来减轻代谢相关脂肪性肝病。

Schisandrin B alleviates metabolic associated fatty liver disease by regulating the PPARγ signaling pathway and gut microbiota in mice.

作者信息

Wan Jiuchen, Lang Chenjian, Gao Meng, Liu Feilong, Feng Xiyuan, Li He, Wang Chunmei, Sun Jinghui

机构信息

School of Pharmacy, Beihua University, Jilin, China.

出版信息

Front Pharmacol. 2025 Jul 25;16:1583307. doi: 10.3389/fphar.2025.1583307. eCollection 2025.

DOI:10.3389/fphar.2025.1583307
PMID:40786039
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12331688/
Abstract

OBJECTIVE: The aim of this study was to investigate the improving effect of Schisandrin B (Sch B) on metabolic associated fatty liver disease (MAFLD) by regulating the PPARγ signaling pathway and gut microbiota, and its mechanism in mice. METHODS: Male C57BL/6 mice were fed with a high-fat diet (HFD) continuously for 16 weeks to establish a MAFLD model. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), and lipopolysaccharide (LPS) in serum, as well as the level of malondialdehyde (MDA), and the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in the liver tissue were measured. Changes in the gut microbiota of mice was analyzed by 16S rRNA sequencing technology. The expression levels of PPARγ, Plin2, Pck1, Acsl4, and Fads1 proteins, as well as those of zonula occludins 1 (ZO-1) and Occludin proteins in the colon tissue were detected by Western Blot. RESULTS: The results showed that Sch B could alleviate the structure disorder, ballooning degeneration, inflammatory cell infiltration, liver lipid droplets, and fibrosis in liver tissue, lower the levels of AST, ALT, TG, TC, LDL-C, and LPS, increase the level of HDL-C and lower the levels of TNF-α and IL-6 in serum, increase the level of IL-10, and lower the level of MDA and increase the activities of SOD and GSH-Px in liver tissue in MAFLD mice. Sch B could increase the expression levels of PPARγ, Pck1, and Fads1 proteins, but decrease Plin2 and Acsl4 proteins in liver tissue. Sch B could improve the diversity and abundance of the gut microbiota, restore the normal composition of the gut microbiota at the phylum and genus levels, alleviate the disruption of the gut barrier caused by HFD, and enhance the expression of ZO-1 and Occludin proteins in colon tissue in MAFLD mice. CONCLUSION: This study showed Sch B can improve HFD-induced MAFLD, and the mechanism may be through regulating the PPARγ, Plin2, PCk1, Acsl4 and Fads1 signaling pathway, restoring the diversity of gut microbiota, and improving the gut barrier to delay the progression of MAFLD.

摘要

目的：本研究旨在探讨五味子乙素（Sch B）通过调节过氧化物酶体增殖物激活受体γ（PPARγ）信号通路和肠道微生物群对代谢相关脂肪性肝病（MAFLD）的改善作用及其在小鼠中的作用机制。 方法：雄性C57BL/6小鼠连续16周高脂饮食（HFD）以建立MAFLD模型。检测血清中天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-10（IL-10）和脂多糖（LPS）水平，以及肝组织中丙二醛（MDA）水平、谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）活性。采用16S rRNA测序技术分析小鼠肠道微生物群的变化。通过蛋白质免疫印迹法检测结肠组织中PPARγ、Plin2、Pck1、Acsl4和Fads1蛋白以及紧密连接蛋白1（ZO-1）和闭合蛋白的表达水平。 结果：结果显示，Sch B可减轻MAFLD小鼠肝组织的结构紊乱、气球样变性、炎性细胞浸润、肝脂质滴和纤维化，降低血清中AST、ALT、TG、TC、LDL-C和LPS水平，升高HDL-C水平，降低TNF-α和IL-6水平，升高IL-10水平，降低肝组织中MDA水平，升高SOD和GSH-Px活性。Sch B可增加肝组织中PPARγ、Pck1和Fads1蛋白的表达水平，但降低Plin2和Acsl4蛋白的表达水平。Sch B可改善肠道微生物群的多样性和丰度，在门和属水平恢复肠道微生物群的正常组成，减轻HFD引起的肠道屏障破坏，并增强MAFLD小鼠结肠组织中ZO-1和闭合蛋白的表达。 结论：本研究表明Sch B可改善HFD诱导的MAFLD，其机制可能是通过调节PPARγ、Plin2、PCk1、Acsl4和Fads1信号通路，恢复肠道微生物群的多样性，改善肠道屏障，从而延缓MAFLD的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c3/12331688/a05fd1b89bcc/fphar-16-1583307-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c3/12331688/17a8ec7055ff/fphar-16-1583307-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c3/12331688/4e39ff207182/fphar-16-1583307-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c3/12331688/e475192861fa/fphar-16-1583307-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c3/12331688/a05fd1b89bcc/fphar-16-1583307-g010.jpg

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Ther Adv Endocrinol Metab. 2023-1-28

[10]
Gut microbiota and its roles in the pathogenesis and therapy of endocrine system diseases.

Microbiol Res. 2023-3

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