Triptolide ameliorates osteoarthritis by regulating nuclear factor kappa B-mediated inflammatory response. (28th February 2022)

• Record Type: Journal Article
• Authors: Liu, Gang; Wang, Laijie; Tuerxunyiming, Muhadasi; Xu, Jin; Wu, Zaifeng; Wang, Wei; Liu, Hongyu; Lin, Lin; Liu, Qingbai
• Is Part Of: Journal of pharmacy and pharmacology. Volume 74:Number 3(2022)
• Page Start: 360
• Page End: 366
• Publication Date: 2022-02-28
• Subjects: osteoarthritis -- chondrocytes -- NF-κB -- inflammatory response; Pharmacy -- Periodicals; Pharmacology -- Periodicals; 615.1
• DOI: 10.1093/jpp/rgab182
• Languages: English
• ISSNs: 0022-3573

Abstract

Abstract: Objectives: Osteoarthritis (OA) is a joint degenerative disease that commonly occurs in older people and affect the quality of life. Triptolide (TPL), a compound derived from Tripterygium wilfordii, has been shown to exhibit anti-inflammatory properties. Here, we investigated the therapeutic effect of TPL on the experimental OA as well as the underlying molecular mechanisms. Methods: OA models were established using monosodium iodoacetate (MIA) or surgery. The arthritis score and paw withdrawal threshold value of knees were used to evaluate the degree of arthritis. The level and expression of proinflammatory cytokines were evaluated by quantitative real-time PCR and ELISA kits. Key findings: In surgery and MIA-induced OA rats, TPL alleviated arthritis symptoms and reduced inflammatory cytokine production in serum. In primary chondrocytes, TPL dose-dependently reversed lipopolysaccharide (LPS)-induced cell proliferation. Moreover, LPS-induced cell apoptosis and the expressions of proinflammatory cytokines interleukin-(IL-)6, IL-8, IL-1β, IL-12, tumour necrosis factor-α (TNF-α) and interferon-gamma (INF-γ) were also attenuated by TPL. Mechanistically, the therapeutic effects of TPL on OA were effective by dampening nuclear factor kappa B (NF-κB) activity leading to reduced proinflammatory cytokines production and inflammatory response. Conclusions: TPL acts as an effective therapeutic drug for OA by mediating NF-κB signalling, thereby leading to the reduced proinflammatory cytokines production and inflammatory response.