茯苓多糖抗非酒精性脂肪肝作用的初步研究

IF 5.1 Q1 CHEMISTRY, APPLIED
Rui Zhou , Qinting Chen , Jie Mo , Meizhen Liu , Ka Wu , Chao Guo
{"title":"茯苓多糖抗非酒精性脂肪肝作用的初步研究","authors":"Rui Zhou ,&nbsp;Qinting Chen ,&nbsp;Jie Mo ,&nbsp;Meizhen Liu ,&nbsp;Ka Wu ,&nbsp;Chao Guo","doi":"10.1016/j.fhfh.2025.100234","DOIUrl":null,"url":null,"abstract":"<div><div>Non-alcoholic fatty liver disease (NAFLD) is a significant public health challenge owing to its current prevalence. Basic and clinical evidence indicates that pyroptosis is responsible for the development of NAFLD to non-alcoholic steatohepatitis. Our previous findings suggested that <em>Poria cocos</em> polysaccharides (PCP) exert promising anti-liver injury benefits. However, the anti-NAFLD action of PCP via the modulation of pyroptosis remains untested. In this study, a network pharmacology- and molecular docking-based approach was used to determine the anti-NAFLD activities and mechanisms of PCP prior to <em>in vitro</em> or <em>in vivo</em>. Based on these bioinformatics data, 31 intersecting genes in PCP (483 target genes), NAFLD (1445 target genes), and pyroptosis (905 target genes) were identified via network pharmacology analysis, and a total of 16 key genes in PCP against NAFLD through the modulation of pyroptosis were determined. Further enrichment analysis revealed the detailed anti-NAFLD functions and molecular mechanisms of PCP. Molecular docking simulations were used to identify the spatial binding features between PCP and the target proteins related to pyroptosis. This study determined the pyroptosis-related cluster genes that act with PCP against NAFLD, thereby offering preliminary evidence to support PCP’s potential in treating NAFLD. Additionally, we identified the possible underlying pyroptotic mechanisms for future experimental validations.</div></div>","PeriodicalId":12385,"journal":{"name":"Food Hydrocolloids for Health","volume":"8 ","pages":"Article 100234"},"PeriodicalIF":5.1000,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The action of Poria cocos polysaccharides against non-alcoholic fatty liver disease: A preliminary study\",\"authors\":\"Rui Zhou ,&nbsp;Qinting Chen ,&nbsp;Jie Mo ,&nbsp;Meizhen Liu ,&nbsp;Ka Wu ,&nbsp;Chao Guo\",\"doi\":\"10.1016/j.fhfh.2025.100234\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Non-alcoholic fatty liver disease (NAFLD) is a significant public health challenge owing to its current prevalence. Basic and clinical evidence indicates that pyroptosis is responsible for the development of NAFLD to non-alcoholic steatohepatitis. Our previous findings suggested that <em>Poria cocos</em> polysaccharides (PCP) exert promising anti-liver injury benefits. However, the anti-NAFLD action of PCP via the modulation of pyroptosis remains untested. In this study, a network pharmacology- and molecular docking-based approach was used to determine the anti-NAFLD activities and mechanisms of PCP prior to <em>in vitro</em> or <em>in vivo</em>. Based on these bioinformatics data, 31 intersecting genes in PCP (483 target genes), NAFLD (1445 target genes), and pyroptosis (905 target genes) were identified via network pharmacology analysis, and a total of 16 key genes in PCP against NAFLD through the modulation of pyroptosis were determined. Further enrichment analysis revealed the detailed anti-NAFLD functions and molecular mechanisms of PCP. Molecular docking simulations were used to identify the spatial binding features between PCP and the target proteins related to pyroptosis. This study determined the pyroptosis-related cluster genes that act with PCP against NAFLD, thereby offering preliminary evidence to support PCP’s potential in treating NAFLD. Additionally, we identified the possible underlying pyroptotic mechanisms for future experimental validations.</div></div>\",\"PeriodicalId\":12385,\"journal\":{\"name\":\"Food Hydrocolloids for Health\",\"volume\":\"8 \",\"pages\":\"Article 100234\"},\"PeriodicalIF\":5.1000,\"publicationDate\":\"2025-07-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Food Hydrocolloids for Health\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2667025925000408\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, APPLIED\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food Hydrocolloids for Health","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667025925000408","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, APPLIED","Score":null,"Total":0}
引用次数: 0

摘要

非酒精性脂肪性肝病(NAFLD)是一个重大的公共卫生挑战,由于其目前的流行。基础和临床证据表明,焦亡是NAFLD发展为非酒精性脂肪性肝炎的原因。我们的研究结果表明茯苓多糖(PCP)具有良好的抗肝损伤作用。然而,PCP通过调节焦亡的抗nafld作用尚未得到验证。在本研究中,采用基于网络药理学和分子对接的方法来确定PCP在体外或体内的抗nafld活性和机制。基于这些生物信息学数据,通过网络药理学分析,鉴定出PCP(483个靶基因)、NAFLD(1445个靶基因)和焦亡(905个靶基因)中31个交叉基因,确定了PCP通过调节焦亡对抗NAFLD的16个关键基因。进一步的富集分析揭示了PCP抗nafld的详细功能和分子机制。通过分子对接模拟,确定PCP与焦亡相关靶蛋白之间的空间结合特征。本研究确定了与PCP一起作用于NAFLD的焦热相关簇基因,从而为支持PCP治疗NAFLD的潜力提供了初步证据。此外,我们为未来的实验验证确定了可能的潜在热亡机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The action of Poria cocos polysaccharides against non-alcoholic fatty liver disease: A preliminary study

The action of Poria cocos polysaccharides against non-alcoholic fatty liver disease: A preliminary study
Non-alcoholic fatty liver disease (NAFLD) is a significant public health challenge owing to its current prevalence. Basic and clinical evidence indicates that pyroptosis is responsible for the development of NAFLD to non-alcoholic steatohepatitis. Our previous findings suggested that Poria cocos polysaccharides (PCP) exert promising anti-liver injury benefits. However, the anti-NAFLD action of PCP via the modulation of pyroptosis remains untested. In this study, a network pharmacology- and molecular docking-based approach was used to determine the anti-NAFLD activities and mechanisms of PCP prior to in vitro or in vivo. Based on these bioinformatics data, 31 intersecting genes in PCP (483 target genes), NAFLD (1445 target genes), and pyroptosis (905 target genes) were identified via network pharmacology analysis, and a total of 16 key genes in PCP against NAFLD through the modulation of pyroptosis were determined. Further enrichment analysis revealed the detailed anti-NAFLD functions and molecular mechanisms of PCP. Molecular docking simulations were used to identify the spatial binding features between PCP and the target proteins related to pyroptosis. This study determined the pyroptosis-related cluster genes that act with PCP against NAFLD, thereby offering preliminary evidence to support PCP’s potential in treating NAFLD. Additionally, we identified the possible underlying pyroptotic mechanisms for future experimental validations.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
4.50
自引率
0.00%
发文量
0
审稿时长
61 days
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信