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.

Beta-amyloid (A beta) plays a key role in the pathogenesis of Alzheimer's disease (AD) by inducing neurotoxicity and cell death mainly through production of reactive oxygen species (ROS). Garcinia mangostana L. (mangosteen) has been recognized as a major source of natural antioxidants that could decrease ROS. However, its role in protection of A beta-induced cytotoxicity and apoptosis in neuronal cells remains unclear. We therefore examined such a protective effect of mangosteen extract (ME) by evaluating cell viability using MTT test, ROS level, caspase-3 activity, and cellular proteome. Treating SK-N-SH cells with 5-20 microM A beta((1-42)) for 24 h caused morphologically cytotoxic changes, decreased cell viability and increased ROS level, whereas preincubation with 50-400 microg/mL ME 30 min before the induction by A beta((1-42)) successfully prevented such cytotoxic effects in a dose-dependent manner (completely at 400 microg/mL). The A beta-induced increase in caspase-3 activity was also preventable by 400 microg/mL ME. Proteomic analysis using 2-D gel electrophoresis (n = 5 gels/group) followed by mass spectrometry revealed 63 proteins whose levels were significantly altered by A beta((1-42)) induction. Interestingly, changes in 10 proteins were successfully prevented by the ME pretreatment. In summary, we report herein the significant protective effects of ME against A beta-induced cytotoxicity, increased ROS, and increased caspase activity in SK-N-SH cells. Moreover, proteomic analysis revealed some proteins that might be responsible for these protective effects by ME. Further characterizations of these proteins may lead to identification of novel therapeutic targets for successful prevention and/or decreasing the severity of AD.

We evaluated the effects of pre-germinated brown rice extract (PGBR ex) with enhanced levels of GABA on proliferation and apoptosis of neuronal SK-N-SH cells line. Firstly, we used HPLC methods to study the level of γ-aminobutyric acid (GABA) in all rice extracts. We found that the concentration of GABA in the PGBR ex were 3 and 8 times higher than the GABA concentration in non-germinated brown rice (BR ex) and white rice (WR ex) compared with the stan- dard GABA respectively. Next we study the protective effects of brown rice extract by investigating various methods, we found that the effects of dose-dependent study by treated with PGBR ex, BR ex and WR ex at (0 - 4000 μg/ml). The data from MTT assay showed that the higher concentration of all rice extracts were not induced toxicity to SK-N-SH cells. To test the protective effect by study the viability of SK-N-SH cells. These results showed that PGBR ex and BR ex can protect cells by significantly increase cells survival up to 29.3% ± 0.01% and13.4% ± 0.07 % (p < 0.05) but not WR ex comparable with 150 ?M H2O2 alone which caused cells death >56.9% ± 0.02 % (p < 0.05), compared with un- treated cells (control). Next study we test the effect of cells apoptotic by ROS assay and DNA fragmentation. The results showed that PGBR ex were definitely decrease the amount of ROS formation and had a little of DNA ladders comparable with condition that induced by 150 ?M H2O2. Our data indicating that PGBR ex with enhanced levels of GABA effectively inhibit SK-N-SH cells proliferation and apoptosis. These present results suggest that intake of PGBR and BR instead of WR is effective to protect cell proliferation and apoptosis which may be useful nutritional to prevent neuronal cells from neurodegenerative disease