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

This 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. The extensive literature from inception to July 2015 was searche...

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Published in:Oncotarget Vol. 7; no. 2; pp. 1193 - 1202
Main Authors: Huang, Qing-Chun, Wang, Mao-Jie, Chen, Xiu-Min, Yu, Wan-Lin, Chu, Yong-Liang, He, Xiao-Hong, Huang, Run-Yue
Format: Journal Article
Language:English
Published: United States Impact Journals LLC 12-01-2016
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Summary:This 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. The extensive literature from inception to July 2015 was searched in PubMed central, and relevant reports were identified according to the purpose of this study. The 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. The 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.
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ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.6200