目的探究摩罗丹浓缩丸(Moluodan concentrated pill,MLD)治疗慢性萎缩性胃炎(chronic atrophic gastritis,CAG)潜在的分子机制。方法利用中药系统药理学数据库与分析平台(Traditional Chinese Medicine Systems Pharmacology Database a...目的探究摩罗丹浓缩丸(Moluodan concentrated pill,MLD)治疗慢性萎缩性胃炎(chronic atrophic gastritis,CAG)潜在的分子机制。方法利用中药系统药理学数据库与分析平台(Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform,TCMSP)、中医药综合数据库(Traditional Chinese Medicine Integrated Database,TCMID)、中医药整合药理学研究平台(Integrative Pharmacologybased Research Platform of Traditional Chinese Medicine,TCMIP)和中药免疫肿瘤学数据库(Traditional Chinese Medicine on Immuno-Oncology,TCMIO)获取MLD的化合物和化合物相关靶点(compound-related target,CRT);DisGeNET和GeneCards数据库获取CAG相关靶点基因(CAG related target gene,CAG-RTG);采用Cytoscape 3.7.2软件构建MLD化合物-CRT网络,并将CRT和CAG-RTG取交集获取MLD相关疾病靶点(MLD-related disease target,MLD-RDT);利用STRING数据库构建MLD-RDT的蛋白质-蛋白质相互作用(protein-protein interaction,PPI)网络,并进行拓扑结构分析,筛选重要靶点。采用基因本体论(Gene Ontology,GO)富集分析与京都基因和基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)信号通路富集分析探索MLD治疗CAG的主要分子机制。结果MLD中共有259个活性分子,获得961个靶基因,其中179个可能与CAG相关。PPI网络显示,AKT1、TNF、IL-6、TP53、IL-1β等是MLD治疗CAG的关键靶点。富集分析显示,MLD治疗CAG的关键通路为PI3K-AKT信号通路和TNF信号通路。结论MLD可能通过介导TNF/PI3K/AKT信号通路治疗CAG。展开更多
Restenosis is a common complication following coronary angioplasty.The traditional use of seaweeds for health benefits has increasingly been explored,however few studies exist reporting its protective effects on the d...Restenosis is a common complication following coronary angioplasty.The traditional use of seaweeds for health benefits has increasingly been explored,however few studies exist reporting its protective effects on the development of restenosis and gut dysbiosis.The aim of this study was to investigate the potential of seaweed extracts(SE) of Ascophyllum nodosum and Fucus vesiculosus in inhibiting intimal hyperplasia in a rat model of restenosis and its underlying mechanisms in macrophages and vascular smooth muscle cells(vSMCs).16S rRNA sequencing was done to investigate the regulatory effect of SE on the gut microbiome of injured rats.As indicated by the results,SE significantly inhibited the progression of intimal hyperplasia in vivo,attenuated inflammation in macrophages and could inhibit the proliferation,dedifferentiation and migration of vSMCs.It was observed through immunoblotting assays that treatment with SE significantly upregulated PTEN expression in macrophages and inhibited the upregulation of PI3K and AKT expression in vSMCs.Meanwhile,according to the 16S rRNA gene sequencing analysis,supplementation with SE modulated gut microbiota composition in injured rats.In conclusion,SE could ameliorate intimal hyperplasia by inhibiting inflammation and vSMCs proliferation through the regulation of the PTEN/PI3K/AKT pathway and modulating the gut microbiome.展开更多
文摘目的探究摩罗丹浓缩丸(Moluodan concentrated pill,MLD)治疗慢性萎缩性胃炎(chronic atrophic gastritis,CAG)潜在的分子机制。方法利用中药系统药理学数据库与分析平台(Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform,TCMSP)、中医药综合数据库(Traditional Chinese Medicine Integrated Database,TCMID)、中医药整合药理学研究平台(Integrative Pharmacologybased Research Platform of Traditional Chinese Medicine,TCMIP)和中药免疫肿瘤学数据库(Traditional Chinese Medicine on Immuno-Oncology,TCMIO)获取MLD的化合物和化合物相关靶点(compound-related target,CRT);DisGeNET和GeneCards数据库获取CAG相关靶点基因(CAG related target gene,CAG-RTG);采用Cytoscape 3.7.2软件构建MLD化合物-CRT网络,并将CRT和CAG-RTG取交集获取MLD相关疾病靶点(MLD-related disease target,MLD-RDT);利用STRING数据库构建MLD-RDT的蛋白质-蛋白质相互作用(protein-protein interaction,PPI)网络,并进行拓扑结构分析,筛选重要靶点。采用基因本体论(Gene Ontology,GO)富集分析与京都基因和基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)信号通路富集分析探索MLD治疗CAG的主要分子机制。结果MLD中共有259个活性分子,获得961个靶基因,其中179个可能与CAG相关。PPI网络显示,AKT1、TNF、IL-6、TP53、IL-1β等是MLD治疗CAG的关键靶点。富集分析显示,MLD治疗CAG的关键通路为PI3K-AKT信号通路和TNF信号通路。结论MLD可能通过介导TNF/PI3K/AKT信号通路治疗CAG。
基金supported by the research grants from the Ministry of Science and Technology of Taiwan (MOST108-2320B-038-040-MY3 and MOST 111-2320-B-038-049)the National Science and Technology Council (NSTC111-2320-B-038-049)。
文摘Restenosis is a common complication following coronary angioplasty.The traditional use of seaweeds for health benefits has increasingly been explored,however few studies exist reporting its protective effects on the development of restenosis and gut dysbiosis.The aim of this study was to investigate the potential of seaweed extracts(SE) of Ascophyllum nodosum and Fucus vesiculosus in inhibiting intimal hyperplasia in a rat model of restenosis and its underlying mechanisms in macrophages and vascular smooth muscle cells(vSMCs).16S rRNA sequencing was done to investigate the regulatory effect of SE on the gut microbiome of injured rats.As indicated by the results,SE significantly inhibited the progression of intimal hyperplasia in vivo,attenuated inflammation in macrophages and could inhibit the proliferation,dedifferentiation and migration of vSMCs.It was observed through immunoblotting assays that treatment with SE significantly upregulated PTEN expression in macrophages and inhibited the upregulation of PI3K and AKT expression in vSMCs.Meanwhile,according to the 16S rRNA gene sequencing analysis,supplementation with SE modulated gut microbiota composition in injured rats.In conclusion,SE could ameliorate intimal hyperplasia by inhibiting inflammation and vSMCs proliferation through the regulation of the PTEN/PI3K/AKT pathway and modulating the gut microbiome.
