[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-406109-105":59,"doc-detail-406109-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","the-study-of-the-therapeutic-effect-and-preliminary-mechanism-of-egcg-on-recurrent-aphthous-ulcer","The study of the therapeutic effect and preliminary mechanism of EGCG on recurrent aphthous ulcer","","The study investigates the pro-healing effect of epigallocatechin gallate (EGCG) on mucosal wounds in recurrent aphthous ulcer (RAU) mice and clarifies underlying molecular mechanisms. A chemical cauterization RAU model was established, and ulcer tissues were analyzed for morphological changes. Network pharmacology predicted targets, while TNF-α and IL-6 were quantified by IHC and ELISA. Western blotting and RT-qPCR evaluated TLR4/MyD88/NF-κB pathway factors, supported by docking and CETSA. Results show EGCG accelerates healing and reduces inflammatory signaling.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/the-study-of-the-therapeutic-effect-and-preliminary-mechanism-of-egcg-on-recurrent-aphthous-ulcer/406109/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/the-study-of-the-therapeutic-effect-and-preliminary-mechanism-of-egcg-on-recurrent-aphthous-ulcer/406109.png","ImageObject",300,407,{"name":92,"@type":93},"Maya Linwood","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-05","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",17,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What was the main objective of the study on EGCG and RAU?","Question",{"text":113,"@type":114},"To assess EGCG’s pro-healing effect on mucosal wounds in RAU mice and to determine its preliminary molecular mechanism.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How was the RAU mouse model established and how were tissues assessed?",{"text":118,"@type":114},"A chemically induced RAU model was created using chemical cauterization, and ulcerated tissues were collected to observe morphological changes.",{"name":120,"@type":111,"acceptedAnswer":121},"Which inflammatory pathway did the results link to EGCG’s mechanism?",{"text":122,"@type":114},"EGCG’s effects were associated with reducing TNF-α and IL-6 and inhibiting the TLR4/MyD88/NF-κB signaling pathway, including lowered TLR4, MyD88, and NF-κB-related factor expressions.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},406109,1790767625,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146,"preview_page_count":4},962084928432,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nThe study of the therapeutic effect and preliminary mechanism of EGCG on recurrent aphthous ulcer  \nXueDi You1,2,7, JunXing Shi5,7, ZhaoXu Ren1,3, Li Wang6 & WanHong Zhao1,4􀀍  \nTo investigate the pro-healing effect of epigallocatechin gallate (EGCG) on mucosal wounds of recurrent aphthous ulcer (RAU) mice and its molecular mechanism. The RAU mouse model was created using chemical cauterization, and ulcerated tissue was collected to observe morphological changes. Network pharmacology identified potential targets and mechanisms. TNF-α and IL-6 levels in ulcer tissues were measured using IHC and ELISA. Western Blotting and RT-qPCR assessed protein and RNA expressions ofTLR4, MYD88, NF-κB, and related factors. A CCK8 assay evaluated the effect of drug concentration on cell activity. Finally, molecular docking and CETSA confirmed the association between EGCG and key target molecules. EGCG has been proven to accelerate the healing of ulcers in ICR mice. Meanwhile, EGCG improved the pathologic morphology of the oral mucosa in mice. A network pharmacological analysis of EGCG’s impact on RAU may be associated with the Toll-like receptor signaling pathway. Simultaneously, the levels ofTNF-α, IL-6, and the expressions ofTLR4, MyD88, p-IKB-α, and p-NF-κBP65/NF-κB P65, NF-κB 1 were decreased. The level of IKB-α was elevated, Showing dose dependence. The EGCG-H group showed better results than the positive control group; EGCG was tightly bound toTLR4 and NF-κB p65 target proteins. In conclusion, EGCG promotes the healing of oral ulcers in RAU mice and increases collagen fiber volume fraction in ulcerated skin tissue. The mechanism may be associated with reducing TNF-α and IL-6 expression levels and inhibiting the TLR4/MyD88/NF-κB signaling pathway.  \nKeywords Epigallocatechin gallate (EGCG), Recurrent aphthous ulcer, Network pharmacology, TLR4/ MyD88/NF-κB pathway, Inflammatory factor  \nAbbreviations  \nEGCG Epigallocatechin gallate  \nRAU Recurrent aphthous ulcer  \nTNF-α Tumor necrosis factor-alpha  \nIL-6 Interleukin-6  \nIHC Immunohistochemistry  \nELISA Enzyme linked immunosorbent assay  \nRT-qPCR Real-time PCR  \nTLR4 Toll-like receptor 4  \nMYD88 Myeloid differentiation primary response protein 88  \nNF-κB Nuclear factor kappa-B  \nNF-κBP65 Nuclear factor kappa-B P65 CCK8 Cell counting Kit-8  \nCETSA Cellular thermal shift assay  \nIKB-α I-kappa-B-alpha  \np-IKB-α p-I-kappa-B-alpha  \n1School of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, Hubei, People’s Republic of China.  \n2Department of Pathology, Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan 442008, Hubei, People’s Republic of China. 3Hubei Key laboratory of Wudang Local Chinese Medicine Research, Shiyan 442000, Hubei, People’s Republic of China. 4Hubei Key Laboratory of Embryonic Stem Cell Research, Shiyan 442000, Hubei, People’s Republic of China. 5Department of Critical Care Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan 442000, Hubei, People’s Republic of China. 6The First Clinical College of Hubei University of Medicine, Shiyan 442000, Hubei, People’s Republic of China. 7XueDiYou and JunXing Shi contributed equally to this work. 􀀍 email: [20090582@hbmu.edu.cn](20090582@hbmu.edu.cn)  \n[www. nature.com/scientificreports/](www. nature.com/scientificreports/)  \nWB  \np-NF-κBP65 HEMASSONGO  \nKEGG  \nPPI  \nWestern blot  \np-Nuclear factor kappa-B P65  \nHematoxylin eosin staining Masson’s trichrome stain Gene ontology  \nKyoto Encyclopedia of Gene and Genome Protein-a protein–protein interaction  \nMouth ulcers are a common chronic disease that affects the oral mucosa. In clinical practice, they are also referred to as recurrent aphthous ulcers (RAU) or recurrent mouth ulcers. RAU is caused by systemic diseases or trauma, such as vitamin deficiencies, disorders ofthe oral microbial system, hematologic factors, stress, genetic diversity, and oxidative-ant","cbCaisjJnL7Y5eU5","https://ap.wps.com/l/cbCaisjJnL7Y5eU5","pdf",3304058,13,"English","# Background\n## Recurrent aphthous ulcer (RAU) overview\n## Current clinical management and limitations\n# Rationale for EGCG\n## EGCG properties and relevance to RAU\n## Inflammation and TLR4/NF-κB signaling\n# Study design and methods\n## RAU mouse model and tissue collection\n## Network pharmacology and target identification\n## Protein/RNA expression analyses (IHC, ELISA, Western blot, RT-qPCR)\n## Cell activity assay and binding validation (CCK8, docking, CETSA)\n# Findings and conclusions\n## Healing and histomorphology improvements\n## Dose dependence and target engagement\n## Proposed mechanism via TLR4/MyD88/NF-κB inhibition","[{\"question\":\"What was the main objective of the study on EGCG and RAU?\",\"answer\":\"To assess EGCG’s pro-healing effect on mucosal wounds in RAU mice and to determine its preliminary molecular mechanism.\"},{\"question\":\"How was the RAU mouse model established and how were tissues assessed?\",\"answer\":\"A chemically induced RAU model was created using chemical cauterization, and ulcerated tissues were collected to observe morphological changes.\"},{\"question\":\"Which inflammatory pathway did the results link to EGCG’s mechanism?\",\"answer\":\"EGCG’s effects were associated with reducing TNF-α and IL-6 and inhibiting the TLR4/MyD88/NF-κB signaling pathway, including lowered TLR4, MyD88, and NF-κB-related factor expressions.\"}]","The study of the therapeutic effect and preliminary mechanism of EGCG on recurrent aphthous ulcer | PDF",1790563596,33]