Mangosteen extracts (ME) contain high levels of polyphenolic compounds and antioxidant activity. Protective effects of ME against β-amyloid peptide (Aβ), induced cytotoxicity have been reported. Here, we further studied the protective effects of ME against oxidative stress induced by hydrogen peroxide (H2O2) and polychlorinated biphenyls (PCBs), and demonstrated the protection against memory impairment in mice. The cytoprotective effects of ME were measured as cell viability and the reduction in ROS activity. In SK-N-SH cell cultures, 200 μg/ml ME could partially antagonize the effects of 150 or 300 µM H2O2 on cell viability, ROS level and caspase-3 activity. At 200, 400 or 800 µg/ml, ME reduced AChE activity of SK-N-SH cells to about 60% of the control. In vivo study, Morris water maze and passive avoidance tests were used to assess the memory of the animals. ME, especially at 100 mg/kg body weight, could improve the animal’s memory and also antagonize the effect of scopolamine on memory. The increase in ROS level and caspase-3 activity in the brain of scopolamine-treated mice were antagonized by the ME treatment. The study demonstrated cytoprotective effects of ME against H2O2 and PCB-52 toxicity and having AChE inhibitory effect in cell culture. ME treatment in mice could attenuate scopolamine-induced memory deficit and oxidative stress in brain.

The different isolated constituents would be further studied for future possible use as chemotherapy in cancer and chemoprevention in Alzheimer's disease.

Mangosteen (Garcinia mangostana L.) is one of the most popular fruits in tropical regions. Mangosteen peel contains several phytochemicals that exhibits antioxidant properties. However, the mechanisms underlying the capacity for mangosteen peel extract (ME) to inhibit cellular oxidative stress have not been fully defined. In this study, we found that ME significantly inhibited hydrogen peroxide (H 2 O 2 )-induced intracellular reactive oxygen species (ROS) production in human neuroblastoma cells (SK-N-SH). Treatment with ME significantly increased the mRNA levels of catalase (CAT) and heme oxygenase-1 in both SK-N-SH and human embryonic kidney (HEK-293) cells. In addition, elevation of CAT enzyme activity was observed in ME-treated SK-N-SH cells. ME possessed significant antioxidant capacities as determined by anti-lipid peroxidation, H 2 O 2 scavenging activity, and 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity assays. We found that(2)-epicatechin and the proanthocyanidin dimer are the active compounds in ME that elicit its antioxidant activities. Practical applicationsMangosteen peel has been traditionally used to treat some illnesses. It contains several phytochemicals, including phenolic compounds and flavonoids which elicit a variety of benefits, including antioxidant and cytoprotective effects. The present study demonstrated that mangosteen peel extract (ME) is a rich source of antioxidants that may have potential uses in nutraceuticals for preventing diseases associated with oxidative stress. K E Y W O R D S antioxidant activity, catalase, epicatechin, heme oxygenase-1, mangosteen peel extract, proanthocyanidin

Mangosteen (Garcinia mangostana L.) a tropical fruit, has been used in traditional medicine. A frequently used part of mangosteen is the pericarp, containing a high content of xanthones. α-Mangostin, one of the major xanthone derivatives, exhibits a variety of actions, including antimicrobial, antioxidant, cytotoxic and antitumor; however, its function on the immune system is still equivocal. This study aimed to examine the immunomodulatory activities of α-mangostin on lymphocyte lineage and cytokine production in human peripheral blood mononuclear cells (PBMCs). The cytotoxic activity of α-mangostin was measured by MTT assay. The concentration of α-mangostin at 5.55 µg/mL resulted in a 50% survival of PBMCs, which was as potent a cytotoxic activity as that of paclitaxel. After 24 h of PBMCs culture, the percentages of T cells (CD3+), B cells (CD19+) and NK cells (CD3-CD16+CD56+) were not significantly changed by treatment with 1, 2 and 4 µg/mL of α-mangostin compared with untreated-PBMCs; in addition, the percentages of these lymphocytes treated with the combination of α-mangostin (1, 2 and 4 µg/mL) and the mitogen concanavalin A (ConA) was not significantly different from that of ConA-treated PBMCs. For cytokine secretion, α-mangostin (1, 2 and 4 µg/mL) did not significantly induce either proinflammatory cytokines (i.e., TNF-α and IL-1β) or cytokine of adaptive immunity (i.e., IL-2). The combination of α-mangostin (1, 2 and 4 µg/mL) and ConA did not significantly alter the relative difference of TNF-α and IL-1β compared with ConA-treated PBMCs; however, these combinations could significantly decrease the relative difference of IL-2 compared with ConAtreated PBMCs. These data indicated that α-mangostin was able to inhibit IL-2 release without interfering with human immune cells; therefore, further studies are necessary to investigate its effect on IL-2 production.

Introduction The water‐soluble mangosteen pericarp extract's (WME) effect was investigated in Alzheimer's disease (AD). Methods The participants received 4 mg/kg/day of WME for 24 weeks (low dose, n = 33), 4 mg/kg/day for 12 weeks and then 8 mg/kg/day for 12 weeks (high dose, n = 33); or a placebo (n = 42). The outcomes were neuropsychiatric test scores, safety, tolerability, and the blood 4‐hydroxynonenal level. Results The proportion of participants who achieved the minimum clinically important difference for the Alzheimer's Disease Assessment Scale–Cognitive Subscale (ADAS‐Cog; –2.6 points) at 24 weeks was significantly higher in the low‐dose group (and a trend in the high‐dose group) than in the placebo group. WME appeared safe and well tolerated. At 24 weeks, the 4‐hydroxynonenal level declined in both intervention groups. The participants with a 5% reduction in this level showed greater ADAS‐Cog improvements. Conclusion WME is a safe and well‐tolerated cognitive enhancer in AD with varying benefits across individuals based on antioxidative response.