Effects of compounds from Garcinia mangostana on inflammatory mediators in RAW264.7 macrophage cells
The fruit hull of Garcinia mangostana Linn. has been used in Thai traditional medicine for treatment of abscess and skin infection. The mangosteen fruit hull and its compounds were carried out to investigate for anti-inflammatory activity. The extract of Garcinia mangostana together with α- and γ-ma...
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Veröffentlicht in: | Journal of ethnopharmacology 2009-01, Vol.121 (3), p.379-382 |
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Sprache: | eng |
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Zusammenfassung: | The fruit hull of
Garcinia mangostana Linn. has been used in Thai traditional medicine for treatment of abscess and skin infection.
The mangosteen fruit hull and its compounds were carried out to investigate for anti-inflammatory activity.
The extract of
Garcinia mangostana together with α- and γ-mangostins were tested for anti-inflammatory effect against lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin E
2 (PGE
2), tumor necrosis factor alpha (TNF-α) and interleukin-4 (IL-4) releases as well as their mechanisms in transcriptional levels using RAW264.7 macrophage cells.
Mangosteen extract possessed potent NO inhibitory effect with an IC
50 value of 1.0
μg/ml. The isolated compounds from the extract including α-mangostin and γ-mangostin, possessed marked inhibitory effect against NO release with IC
50 values of 3.1 and 6.0
μM, respectively. The extract exhibited potent inhibitory effect on PGE
2 release (IC
50
=
6.0
μg/ml), whereas those of α- and γ-mangostins were 13.9 and 13.5
μM, respectively. However, mangostins possessed only moderate effects towards TNF-α and IL-4 releases with IC
50 values ranging from 31.8 to 64.8
μM. Both extract and α-mangostin suppressed transcription of gene encoding inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in dose-dependent manners, whereas γ-mangostin had only an inhibitory effect on transcription of iNOS.
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 PGE
2 releases, but moderate effect through TNF-α and IL-4. |
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ISSN: | 0378-8741 1872-7573 |
DOI: | 10.1016/j.jep.2008.11.007 |