Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?

Abstract

OBJECTIVESThis review stated the possible application of the active components of licorice, glycyrrhizin (GL) and glycyrrhetinic acid (GA), in rheumatoid arthritis (RA) treatment based on the cyclooxygenase (COX)-2/thromboxane A2 (TxA2) pathway.METHODSThe extensive literature from inception to July 2015 was searched in PubMed central, and relevant reports were identified according to the purpose of this study.RESULTSThe active components of licorice GL and GA exert the potential anti-inflammatory effects through, at least in part, suppressing COX-2 and its downstream product TxA2. Additionally, the COX-2/TxA2 pathway, an auto-regulatory feedback loop, has been recently found to be a crucial mechanism underlying the pathogenesis of RA. However, TxA2 is neither the pharmacological target of non-steroidal anti-inflammatory drugs (NSAIDs) nor the target of disease modifying anti-rheumatic drugs (DMARDs), and the limitations and side effects of those drugs may be, at least in part, attributable to lack of the effects on the COX-2/TxA2 pathway. Therefore, GL and GA capable of targeting this pathway hold the potential as a novel add-on therapy in therapeutic strategy, which is supported by several bench experiments.CONCLUSIONSThe active components of licorice, GL and GA, could not only potentiate the therapeutic effects but also decrease the adverse effects of NSAIDs or DMARDs through suppressing the COX-2/TxA2 pathway during treatment course of RA.

Chinese Herbal Medicines for Rheumatoid Arthritis: Text‐Mining the Classical Literature for Potentially Effective Natural Products

“…In reflection of the frequent clinical application of these herbs in combination with conventional medications, some studies have examined combined effects. For example, compounds from Glycyrrhiza uralensis Fisch have been reported to enhance the therapeutic effects of NSAIDs and DMARDs [68], and the compound ligustrazine derived from Ligusticum chuanxiong Hort. was reported to reduce bone cortex erosion when combined with leflunomide in a clinical study [99].…”

“…6 Evidence-Based Complementary and Alternative Medicine Liquiritin [66], glycyrol [67], glycyrrhizin, glycyrrhetinic acid [68] (i) Anti-inflammatory [66][67][68], (ii) restrained angiogenesis [66], (iii) down-regulated autoimmune reactions [67], (iv) enhanced therapeutic effects of NSAIDs/DMARDs [68] Jiang, Sheng jiang, Gan jiang…”

Herbal compounds for rheumatoid arthritis: Literatures review and cheminformatics prediction

“…Some previous researches have shown that betulinic acid, kaempferol, leonurine, oxymatrine, and piperlongumine can inhibit the migration and invasion of FLS in RA models (Li et al, ; Liang et al, ; Liu, Feng, et al, ; Pan et al, ; Sun, Xu, Du, Zhang, & Zhu, ). Triptolide, celastrol, geniposide, paeoniflorin, clematichinenoside AR, glycyrrhetinic acid, kirenol, cucurbitacin E, 1,7‐dihydroxyl‐3,4‐dimethoxylxanthone, calycosin, catechin, cyanidin‐3‐glucoside, quercetin, α‐mangostin, leonurine, norisoboldine, oxymatrine, caffeic acid, paeonol, resveratrol, shikonin, and 3 R ‐(4′‐hydroxyl‐3′‐ O ‐β‐ d ‐glucopyranosyl phenyl)‐dihydro isocoumarin alleviate inflammatory response by inhibiting the release of a variety of proinflammatory factors (e.g., activin A, ciliary neurotrophic factor, and fractalkine) in FLS of RA models (Bi et al, ; Chen et al, ; Deng et al, ; Huang et al, ; Jia et al, ; Li et al, ; Liang et al, ; Lin, Sato, & Ito, ; Liu, Feng, et al, ; Mao, Sun, Pei, & Zhang, ; Su et al, ; Su et al, ; Sun et al, ; Sun et al, ; Sun & Li, ; Sung et al, ; Tang et al, ; Tian, Chen, Gao, Li, & Xie, ; Venkatesha, Astry, Nanjundaiah, Yu, & Moudgil, ; Wang, Sun, & Jin, ; Wei et al, ; Yang et al, ; Yang et al, ; Zhang et al, ; Zheng et al, ; Zuo et al, ).…”

“…Multiple inflammatory indices (e.g., TNF‐α, IL‐1, and IL‐6) are dysregulated in the peripheral blood of RA patients, which may also participate in the mechanisms of some constituents against RA, including triptolide; paeoniflorin; artesunate; artemether; glycyrrhizin; madecassoside; taraxasterol; apigenin; luteolin; quercetin; 1,7‐dihydroxyl‐xanthone; 2‐hydroxyl‐1,7‐dimethoxylxanthone; 1,7‐dihydroxyl‐3,4‐dimethoxylxanthone; berberine; norisoboldine; oxymatrine; sinomenine; curculigoside A; curcumin; ferulic acid; p‐coumaric acid; daphnetin; and matrine (Cai, Zheng, Shang, Zhao, & R., Y., ; Cuzzocrea, Saadat, Di Paola, & Mirshafiey, ; Ding et al, ; Gao, Shan, Di, Jiang, & Xu, ; Huang et al, ; Impellizzeri et al, ; Jia & He, ; Jiang, Ping, Sun, Wang, & Sun, ; Li et al, ; Lin et al, ; Luo et al, ; Ma et al, ; Pu et al, ; Shi, Zhou, Ji, Xu, & Yang, ; Tu, Hu, & Lu, ; Wang et al, ; Wang, Mo, & Zhang, ; Yang, Zhang, et al, ; Zhai et al, ; Zheng et al, ; Zhou, Wong, Wang, Cai, & Liu, ; Zhu et al, ; Zhu et al, ; Zuo, Xia, Li, & Chen, ). In addition, some kinds of cells in peripheral blood are also involved in the inflammatory processes of RA.…”

18β-Glycyrrhetinic acid protects against alpha-naphthylisothiocyanate-induced cholestasis through activation of the Sirt1/FXR signaling pathway

“…18β-Glycyrrhetinic acid (18b-GA) is a product of glycyrrhizin metabolism through the intestinal flora [11]. 18b-GA has recently been reported to have anti-inflammatory [12], anticancer [13,14], and hepatoprotective [15] effects. In addition, recent evidence indicates that 18b-GA exerts a powerful protective effect in multiple liver injury models, including models of exposure to free fatty acids [16], BA [9], a choline-deficient L-amino acid-defined diet [17], and carbon tetrachloride [18].…”