{"title":"Activation of the NF-κB signaling pathway by Reynoutria japonica Houtt ameliorates complete Freund's adjuvant-induced arthritis in rats.","authors":"Xiao-Feng Li, Xiongwu Yang, Hui Gao","doi":"10.1007/s10787-025-01662-9","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) manifests through persistent synovitis and systemic inflammation, which ultimately result in the degradation of cartilage and bone. The current study was to scrutinize the anti-arthritic effect of Reynoutria japonica Houtt ameliorating complete Freund's adjuvant (CFA)-induced RA in rats and explore the underlying mechanism.</p><p><strong>Material and methods: </strong>CFA was used for the induction of RA in the rats (rats were received the oral administration of Reynoutria japonica Houtt) and estimation of body weight and organ weight. The paw volume, arthritic score, paw withdrawn threshold, and paw withdrawn latency were estimated at regular time. The RF, hematological, hepatic, non-hepatic, ATG, oxidative stress, cytokines, and inflammatory parameters were estimated. The mRNA expression of different genes was scrutinized.</p><p><strong>Results: </strong>Reynoutria japonica Houtt treatment improved the body weight and reduced the spleen and thymus index. Reynoutria japonica Houtt also suppressed the paw edema, arthritic score, paw withdrawn threshold, and paw withdrawn latency at regular time interval. Reynoutria japonica Houtt suppressed the RF and altered the hematological, hepatic, non-hepatic, cytokines and inflammatory parameters. Reynoutria japonica Houtt treatment significantly (P < 0.001) altered the expression of MMP-2, MMP-9, MMP-12, TNF-α, IL-1β, Il-6, IL-10, IL-17, COX-1, COX-2, NF-κB, iNOS, mTOR, LC3-II, AMPK, and Beclin 1.</p><p><strong>Conclusion: </strong>The result clearly stated the promising effect of Reynoutria japonica Houtt against CFA-induced RA in rats via the suppression of NF-κB signaling pathway.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1407-1424"},"PeriodicalIF":4.6000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammopharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10787-025-01662-9","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/2/19 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Rheumatoid arthritis (RA) manifests through persistent synovitis and systemic inflammation, which ultimately result in the degradation of cartilage and bone. The current study was to scrutinize the anti-arthritic effect of Reynoutria japonica Houtt ameliorating complete Freund's adjuvant (CFA)-induced RA in rats and explore the underlying mechanism.
Material and methods: CFA was used for the induction of RA in the rats (rats were received the oral administration of Reynoutria japonica Houtt) and estimation of body weight and organ weight. The paw volume, arthritic score, paw withdrawn threshold, and paw withdrawn latency were estimated at regular time. The RF, hematological, hepatic, non-hepatic, ATG, oxidative stress, cytokines, and inflammatory parameters were estimated. The mRNA expression of different genes was scrutinized.
Results: Reynoutria japonica Houtt treatment improved the body weight and reduced the spleen and thymus index. Reynoutria japonica Houtt also suppressed the paw edema, arthritic score, paw withdrawn threshold, and paw withdrawn latency at regular time interval. Reynoutria japonica Houtt suppressed the RF and altered the hematological, hepatic, non-hepatic, cytokines and inflammatory parameters. Reynoutria japonica Houtt treatment significantly (P < 0.001) altered the expression of MMP-2, MMP-9, MMP-12, TNF-α, IL-1β, Il-6, IL-10, IL-17, COX-1, COX-2, NF-κB, iNOS, mTOR, LC3-II, AMPK, and Beclin 1.
Conclusion: The result clearly stated the promising effect of Reynoutria japonica Houtt against CFA-induced RA in rats via the suppression of NF-κB signaling pathway.
期刊介绍:
Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas:
-Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states
-Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs
-Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents
-Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain
-Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs
-Muscle-immune interactions during inflammation [...]