Pycnogenol attenuates the symptoms of immune dysfunction through restoring a cellular antioxidant status in low micronutrient-induced immune deficient mice

BACKGROUND/OBJECTIVES: We investigated the effect of Pycnogenol (Pyc) on survival and immune dysfunction of C57BL/6 mice induced by low micronutrient supplementation. MATERIALS/METHODS: Female C57/BL/6 mice were fed a diet containing 7.5% of the recommended amount of micronutrients for a period of 12 wks (immunological assay) and 18 wks (survival test). For immunological assay, lymphocyte proliferation, cytokine regulation, and hepatic oxidative status were determined. RESLUTS: Pyc supplementation with 50 and 100 mg.kg(-1).bw.d(-1) resulted in partial extension of the median survival time. Pyc supplementation led to increased T and B cell response against mitogens and recovery of an abnormal shift of cytokine pattern designated by the decreased secretion of Th1 cytokine and increased secretion of Th2 cytokine. Hepatic vitamin E level was significantly decreased by micronutrient deficiency, in accordance with increased hepatic lipid peroxidation level. However, Pyc supplementation resulted in a dose-dependent reduction of hepatic lipid peroxidation, which may result from restoration of hepatic vitamin E level. CONCLUSION: Findings of this study suggest that Pyc supplementation ameliorates premature death by restoring immune dysfunction, such as increasing lymphocyte proliferation and regulation of cytokine release from helper T cells, which may result from the antioxidative ability of Pyc.

Epigallocatechin gallate attenuates L-DOPA-induced apoptosis in rat PC12 cells

In this study, the protective effects of EGCG on L-3,4-dihydroxyphenylalanine (L-DOPA)-induced oxidative cell death in catecholaminergic PC12 cells, the in vitro model of Parkinson's disease, were investigated. Treatment with L-DOPA at concentrations higher than 150 microM caused cytotoxicity in PC12 cells, as determined using the 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry detection. The apoptotic ratio was similar in cells treated with 100 microM EGCG plus 150 microM L-DOPA (5.02%) and the control (0.96%) (P > 0.05), and was lower than that of cells treated with L-DOPA only (32.24%, P < 0.05). The generation level of ROS (% of control) in cells treated with EGCG plus L-DOPA was lower than that in cells treated with L-DOPA only (123.90% vs 272.32%, P < 0.05). The optical density in production of TBARS in cells treated with L-DOPA only was higher than that in the control (0.27 +/- 0.05 vs 0.08 +/- 0.04, P < 0.05), and in cells treated with EGCG only (0.14 +/- 0.02, P < 0.05), and EGCG plus L-DOPA (0.13 +/- 0.02, P < 0.05). The intracellular level of GSH in cells treated with EGCG plus L-DOPA was higher than that in cells treated with L-DOPA only (233.25 +/- 16.44 vs 119.23 +/- 10.25, P < 0.05). These results suggest that EGCG protects against L-DOPA-induced oxidative apoptosis in PC12 cells, and might be a potent neuroprotective agent.