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Review
. 2017 Jan 6;9(1):45.
doi: 10.3390/nu9010045.

Resveratrol, Potential Therapeutic Interest in Joint Disorders: A Critical Narrative Review

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Free PMC article
Review

Resveratrol, Potential Therapeutic Interest in Joint Disorders: A Critical Narrative Review

Christelle Nguyen et al. Nutrients. .
Free PMC article

Abstract

Trans-resveratrol (t-Res) is a natural compound of a family of hydroxystilbenes found in a variety of spermatophyte plants. Because of its effects on lipids and arachidonic acid metabolisms, and its antioxidant activity, t-Res is considered as the major cardioprotective component of red wine, leading to the "French Paradox" health concept. In the past decade, research on the effects of resveratrol on human health has developed considerably in diverse fields such as cancer, neurodegenerative and cardiovascular diseases, and metabolic disorders. In the field of rheumatic disorders, in vitro evidence suggest anti-inflammatory, anti-catabolic, anti-apoptotic and anti-oxidative properties of t-Res in various articular cell types, including chondrocytes and synoviocytes, along with immunomodulation properties on T and B lymphocytes. In preclinical models of osteoarthritis and rheumatoid arthritis, resveratrol has shown joint protective effects, mainly mediated by decreased production of pro-inflammatory and pro-degradative soluble factors, and modulation of cellular and humoral responses. Herein, we comprehensively reviewed evidence supporting a potential therapeutic interest of t-Res in treating symptoms related to rheumatic disorders.

Keywords: aryl hydrocarbon receptor; chondrocyte; inflammation; osteoarthritis; pain; rheumatoid arthritis; synoviocytes; trans-resveratrol.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The pleiotropic effects of t-Resveratrol (t-Res). AKT: Protein kinase B; AMPK: 5' adenosine monophosphate-activated protein kinase; AP-1: Activator protein 1; COX: cyclooxygenase; ER: estrogen receptor; ERK1/2: Extracellular signal-regulated protein kinases 1 and 2; IL-1β: Interleukin-1β; MAPK: Mitogen-activated protein kinase; MEK: Mitogen-activated protein kinase kinase; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; R: receptor; Th: T helper; TNF-α: Tumour necrosis factor-α.
Figure 2
Figure 2
Aryl hydrocarbon and dioxin receptor (AhR)—a new target of IL-1β in chondrocytes. Rabbit chondrocytes were cultured in the absence (A) or in the presence (B) of IL-1β (5 nM) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Ligand was added to the cells for 20 h. AhR expression was studied by immunocytochemistry. (A) In the absence of IL-1β, the AhR signal is restricted to the cytoplasmic area of chondrocytes. Addition of TCDD does not modify the AhR signal; (B) In contrast, in the presence of IL-1β, addition of TCDD induces AhR translocation to the nucleus; (C) IL-1β-increased expression of AhR over control values was shown to occur through AP1 activation and followed by robust expression of CYP1A1 (Widerak M, Corvol MT and Savouret JF, personal data).
Figure 3
Figure 3
The anti-AhR effect of active metabolites of t-Res in chondrocytes could be more effective in the presence of pro-inflammatory cytokines.

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