{"title":"outtuynia cordatapolysaccharide attenuates LPS-induced lung injury by inhibiting the HMGB3/JNK pathway through upregulation of miR-200b-3p","authors":"Wei Hong Liu, Li Yan Yin, Bao Gang Wang","doi":"10.37360/blacpma.25.24.5.55","DOIUrl":null,"url":null,"abstract":"The aim was toinvestigate the therapeutic effects and molecular mechanisms of Houttuynia cordatapolysaccharide (HCP) on LPS-induced lung injury.Effects were analyzed by HE, TUNEL, ELISA, MTT, and flow cytometry. Roles and mechanisms of HCP, miR-200b-3p, HMGB3, and JNK were studied by RT-qPCR, Western Blot, transfection, and dual luciferase reporter gene.HCP treatment effectively ameliorated LPS-induced lung injury in mice and TC-1 cells and was able to inhibit inflammatory factors as well as apoptosis with an effect close to that of dexamethasone-positive control. miR-200b-3p expression was down-regulated in LPS-induced lung injury and up-regulated by HCP treatment, and miR-200b-3p inhibitors reduced the therapeutic effects of HCP. miR-200b-3p targeted and negatively regulated HMGB3. HMGB3 was able to activate the JNK pathway to suppress the therapeutic effects of HCP on lung cell injury.HCP attenuates LPS-induced lung injury by upregulating miR-200b-3p to inhibit the HMGB3/JNK pathway.","PeriodicalId":55342,"journal":{"name":"Boletin Latinoamericano y del Caribe de Plantas Medicinales y Aromaticas","volume":"24 5","pages":"790-814"},"PeriodicalIF":0.8000,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.blacpma.ms-editions.cl/index.php/blacpma/article/download/524/556/1042","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Boletin Latinoamericano y del Caribe de Plantas Medicinales y Aromaticas","FirstCategoryId":"0","ListUrlMain":"https://doi.org/10.37360/blacpma.25.24.5.55","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"INTEGRATIVE & COMPLEMENTARY MEDICINE","Score":null,"Total":0}
引用次数: 0
Abstract
The aim was toinvestigate the therapeutic effects and molecular mechanisms of Houttuynia cordatapolysaccharide (HCP) on LPS-induced lung injury.Effects were analyzed by HE, TUNEL, ELISA, MTT, and flow cytometry. Roles and mechanisms of HCP, miR-200b-3p, HMGB3, and JNK were studied by RT-qPCR, Western Blot, transfection, and dual luciferase reporter gene.HCP treatment effectively ameliorated LPS-induced lung injury in mice and TC-1 cells and was able to inhibit inflammatory factors as well as apoptosis with an effect close to that of dexamethasone-positive control. miR-200b-3p expression was down-regulated in LPS-induced lung injury and up-regulated by HCP treatment, and miR-200b-3p inhibitors reduced the therapeutic effects of HCP. miR-200b-3p targeted and negatively regulated HMGB3. HMGB3 was able to activate the JNK pathway to suppress the therapeutic effects of HCP on lung cell injury.HCP attenuates LPS-induced lung injury by upregulating miR-200b-3p to inhibit the HMGB3/JNK pathway.
期刊介绍:
The Boletín Latinoamericano y del Caribe de Plantas Medicinales y Aromáticas (BLACPMA), [Latin American and Caribbean Bulletin of Medicinal and Aromatic Plants]; currently edited by the publishing house MS-Editions, is a bi-monthly international publication that publishes original peerreviewed research in the field of medicinal and aromatic plants, with nearly 20 years of experience. BLACPMA is a scientific journal that publishes two types of articles: Reviews (only in English) and Original Articles (Spanish or English), its main lines of action being agronomy, anthropology and ethnobotany, industrial applications, botany, quality and standardization, ecology and biodiversity, pharmacology, phytochemistry, pharmacognosy, regulatory and legislative aspects. While all areas of medicinal plants are welcome and the experimental approaches used can be broad and interdisciplinary; other areas of research that are not mentioned depend on the Editorial Committee for their acceptance.