Abstract
Astilbin, a flavonoid compound, was isolated from the rhizome of Smilax glabra Roxb. (with red cross-section) grown in Guizhou Province, China. We accessed its effect and potential mechanism on attenuation of the inflammatory response in CFA-induced AA rats. Our results showed that daily oral administration of astilbin at 5.3 mg/kg reduced joint damage in the hind paw of AA rats. Accordingly, astilbin exhibited remarkable inhibitory effects on TNF-α, IL-1β, and IL-6 mRNA expression. Significant decrease of serum cytokine levels of TNF-α, IL-1β, and IL-6 was also observed in astilbin-treated AA rats compared to the vehicle-treated AA rats. The reduced expression of these cytokines was associated with protein activity suppression of three key molecular targets in the pathogenesis of RA, including IKKβ, NF-κB p65 subunit, and TLR adaptor MyD88. Furthermore, the therapeutic effects of astilbin on the inhibition of cytokines production as well as the reduction of inflammatory response in AA rats are close to a commonly used antirheumatic drug, leflunomide. Collectively, our data suggest that the action mechanism of astilbin, as an anti-inflammatory agent for RA treatment, is associated with modulating the production of proinflammatory cytokines and inhibiting the expression of key elements in NF-κB signaling pathway mediated by TLR.
Highlights
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints, associated with inflammatory infiltration of the synovia, and cartilage/bone destruction
In the soft X-ray examination, a marked reduction of swelling in the hind paw was seen in the astilbin-treated adjuvant arthritis (AA) rats
The decrease of joint lesions was confirmed by histological examination on day 21 after astilbin administration (Figure 3): treatment with astilbin led to a significant inhibition of inflammatory cell infiltration against adjuvant-induced arthritis in rats
Summary
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints, associated with inflammatory infiltration of the synovia, and cartilage/bone destruction. It affects nearly 1% of the population worldwide [1]. Inflamed synovial tissues are infiltrated by monocyte/macrophage, synovial fibroblast, T cells, and B cells, which are considered as key players in the mammalian immune system [4] In response to such immune/inflammatory stimuli, proinflammatory cytokines, including but not limited to tumor necrosis factorα (TNF-α), interleukin-1 (IL-1), and IL-6, are subsequently released by these cells [5]. Due to their important roles in the pathogenesis of RA, cytokines have
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