Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?
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Qing-Chun Huang1, Mao-Jie Wang2, Xiu-Min Chen1, Wan-Lin Yu2, Yong-Liang Chu1, Xiao-Hong He1 and Run-Yue Huang1
1 Department of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China
2 Central Laboratory, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China
Run-Yue Huang, email:
Keywords: licorice, glycyrrhizin, glycyrrhetinic acid, rheumatoid arthritis, the COX-2/TxA2 pathway
Received: August 03, 2015 Accepted: October 09, 2015 Published: October 20, 2015
OBJECTIVES: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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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