− Inflammation plays an important role in host defense against external stimuli such as infection by pathogen, endotoxin or chemical exposure by the production of the inflammatory mediators that produced by macrophage. Anti-inflammatory factor is important to treat the dangers of chronic inflammation associated with chronic disease. This research aims to analyze the anti-inflammatory effects of Garcinia mangostana L. peel extract (GMPE), α-mangostin, and γ-mangostin in LPS-induced murine macrophage cell line (RAW 264.7) by inhibiting the production of inflammatory mediators. The cytotoxic assay of G. mangostana L. extract, α-mangostin, and γ-mangostin were performed by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) to determine the safe and non-toxic concentration in RAW 264.7 for the further assay. The concentration of inflammatory mediators (COX-2, IL-6, and IL-1β) were measured by the ELISA-based assay and NO by the nitrate/nitrite colorimetric assay in treated LPS-induced RAW 264.7 cells. The inhibitory activity was determined by the reducing concentration of inflammatory mediators in treated LPS-induced RAW 264.7 over the untreated cells. This research revealed that GMPE, α-mangostin, and γ-mangostin possess the anti-inflammatory effect by reducing COX-2, IL-6, IL-1β, and NO production in LPS-induces RAW 264.7 cells.

Atherosclerosis as one of the causes of cardiovascular disease will induce endothelial dysfunction and platelet aggregation. Mangostin peel extract (MPE) contains xanthones which have antioxidant activity, anti-cholesterol, anti-aggregation, and anti-inflammatory in preventing and inhibiting atherosclerosis. In this research, MPE was evaluated the xanthones quantitative based on standard xanthone compounds using High Liquid Performance Chromatography (HPLC) method and tested anti-aggregation platelet activity and ABTS+ 2,2-Azinobis-(3 ethylbenzothiazoline-6-sulfonic acid) diammonium (ABTS)-reducing activity. The anti-aggregation platelet using agonist namely adenosine diphosphate inducer (ADP), collagen (COLL), and epinephrine (EPN). Quantification of MPE using four xanthones compound as a marker, showed that MPE contained α-mangostin 105 ppm, γ-mangostin 7.20 ppm, 9.92 ppm Gar-C, and Gar-D 3.50 ppm. MPE and xathones had high ABTS-reducing activity and the most active was, α-mangostin with IC50 2.348 µg/ml. α-mangostin and γ-mangostin had anti-aggregation activity on EPN inducer were comparable with aspirin. MPE and xathones had no anti-aggregation activity on COLL and ADP inducer. MPE contain xathones including α-mangostin, γ-mangostin, Garcinone-C and Garcinone-D. MPE and xanthones have high ABTSreducing activity. MPE, α-mangostin, γ-mangostin, Garcinone-D decrease EPN-induced aggregation platelet. α-mangostin, γ-mangostin were the most active antia-ggregation and antioxidant activities.

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Obesity is one of the risk factors for atherosclerosis and its fat occurrence and development are associated with fat accumulation and adipocyte differentiation.  Thus, the suppression of adipocyte differentiation can be a potential anti-obesity approach to this health concern. This study examined the effect of mangosteen pericarp extract (MPE) and xanthone (α-Mangostin (AM) and γ-Mangostin (GM)) on the expression of PPARγ, C/EBPα, SCD1, LPL, aP2, adipoQ, and FAS in 3T3-L1 cells. Concentrations of MPE and xanthones used were based on the cytotoxic assay on 3T3-L1 cells. Three different MPE concentrations (0, 25, and 50 µg/ml) and three different AM concentrations (0, 25 and 50 µM) and GM (0, 50, and 75 µM) were used in the experiment. The expressions of PPARγ, C/EBPα, SCD1, LPL, aP2, adipoQ, and FAS genes were measured using real-time quantitative PCR. The expression of the genes was down-regulated in the group of cells treated with 50 µg/ml of MPE and 50 µM of GM. However, the 25 µM and 50 µM of AM did not suppress PPARγ and SCD-1 expression. The 50 µM of AM also failed to reduce aP2 gene expression. Finally, MPE and GM showed potential anti-adipogenesis and anti-obesity effects by suppressing the expression of PPARγ, C/EBPα, SCD1, LPL, aP2, adipoQ and FAS genes in 3T3-L1 cells.

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