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Effects of compounds from Garcinia mangostana on inflammatory mediators in RAW264.7 macrophage cells
Supinya Tewtrakul1, Chatchai Wattanapiromsakul, Wilawan Mahabusarakam
1Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Prince of Songkla University, Hat-Yai, Songkhla 90112, Thailand. supinyat@yahoo.com
Ethnopharmacological Relevance:
The fruit hull of Garcinia mangostana Linn. has been used in Thai traditional medicine for treatment of abscess and skin infection.
Aim Of The Study:
The mangosteen fruit hull and its compounds were carried out to investigate for anti-inflammatory activity.
Material And Methods:
The extract of Garcinia mangostana together with alpha- and gamma-mangostins were tested for anti-inflammatory effect against lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha) and interleukin-4 (IL-4) releases as well as their mechanisms in transcriptional levels using RAW264.7 macrophage cells.
Results:
Mangosteen extract possessed potent NO inhibitory effect with an IC50 value of 1.0 microg/ml. The isolated compounds from the extract including alpha-mangostin and gamma-mangostin, possessed marked inhibitory effect against NO release with IC50 values of 3.1 and 6.0 microM, respectively. The extract exhibited potent inhibitory effect on PGE2 release (IC50=6.0 microg/ml), whereas those of alpha- and gamma-mangostins were 13.9 and 13.5 microM, respectively. However, mangostins possessed only moderate effects towards TNF-alpha and IL-4 releases with IC50 values ranging from 31.8 to 64.8 microM. Both extract and alpha-mangostin suppressed transcription of gene encoding inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in dose-dependent manners, whereas gamma-mangostin had only an inhibitory effect on transcription of iNOS.
Conclusion:
The present study may support the Thai traditional use of Garcinia mangostana fruit hull for treatment of inflammatory-related diseases through the inhibition of NO and PGE2 releases, but moderate effect through TNF-alpha and IL-4.