{"title":"<i>Morinda umbellata</i> active fraction inhibits lipopolysaccharide induced proinflammatory cytokines by downregulating <i>NF-κB</i> activation.","authors":"Neenthamadathil Mohandas Krishnakumar, Kuttapetty Manikantan, Somasekharan Nair Rajam Suja, Panickamparambil Gopalakrishnan Latha, Stanislaus Antony Ceasar","doi":"10.1093/toxres/tfac063","DOIUrl":null,"url":null,"abstract":"<p><p><i>Morinda umbellata</i> L. is a woody climber or liana distributed in south East Asia. It is a traditional medicinal plant with excellent curative effects against diarrhea, dysentery, and other stomach disorders. The present study was aimed to assess the effect of <i>M. umbellata</i> active fraction (MUAF) on various inflammatory mediators using lipopolysaccharide (LPS) induced <i>in vivo</i> model in Wistar rats. The effect of MUAF on secretion of TNF-α, IL-1β, and IL-6 were evaluated in LPS-induced experimental animals. The expression of <i>TNF-</i>α<i>, IL-1β, IL-6, iNOS, COX-2</i>, and <i>nuclear factor NF-κB</i> genes were also evaluated. The gas chromatography-mass spectrometry (GC-MS) analysis of the active fraction was carried out to identify the active compounds present in MUAF. The results of oral acute toxicity suggested the non-toxic nature of MUAF. GC-MS analysis of the MUAF leaves revealed the presence of 8 compounds. The study demonstrated that the proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 were significantly inhibited by MUAF in a dose-dependent manner. Moreover, MUAF down-regulated the expression of <i>TNF-</i>α<i>, IL-1β, IL-6, iNOS, COX-2</i>, and <i>NF-κB</i> genes. Our research findings suggest that the presence of anti-inflammatory compounds in MUAF can effectively inhibit LPS-induced proinflammatory cytokines TNF-α, IL-β, and IL-6 <i>in vivo</i>. It also suppressed the over expression of <i>TNF-</i>α, <i>IL-1β</i>, <i>IL-6</i>, <i>iNOS</i>, and <i>COX-2</i> possibly via downregulating <i>NF-κB</i> activation.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"11 5","pages":"841-851"},"PeriodicalIF":2.2000,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9618104/pdf/tfac063.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfac063","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Morinda umbellata L. is a woody climber or liana distributed in south East Asia. It is a traditional medicinal plant with excellent curative effects against diarrhea, dysentery, and other stomach disorders. The present study was aimed to assess the effect of M. umbellata active fraction (MUAF) on various inflammatory mediators using lipopolysaccharide (LPS) induced in vivo model in Wistar rats. The effect of MUAF on secretion of TNF-α, IL-1β, and IL-6 were evaluated in LPS-induced experimental animals. The expression of TNF-α, IL-1β, IL-6, iNOS, COX-2, and nuclear factor NF-κB genes were also evaluated. The gas chromatography-mass spectrometry (GC-MS) analysis of the active fraction was carried out to identify the active compounds present in MUAF. The results of oral acute toxicity suggested the non-toxic nature of MUAF. GC-MS analysis of the MUAF leaves revealed the presence of 8 compounds. The study demonstrated that the proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 were significantly inhibited by MUAF in a dose-dependent manner. Moreover, MUAF down-regulated the expression of TNF-α, IL-1β, IL-6, iNOS, COX-2, and NF-κB genes. Our research findings suggest that the presence of anti-inflammatory compounds in MUAF can effectively inhibit LPS-induced proinflammatory cytokines TNF-α, IL-β, and IL-6 in vivo. It also suppressed the over expression of TNF-α, IL-1β, IL-6, iNOS, and COX-2 possibly via downregulating NF-κB activation.