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Antioxidant Activity and Protective Effects of <Emphasis Type="Italic">Tripterygium regelii</Emphasis> Extract on Hydrogen Peroxide-Induced Injury in Human Dopaminergic Cells,SH-SY5Y
Authors:Bong-Suk Choi  Kumar Sapkota  Seung Kim  Hyo Jeong Lee  Han-Seok Choi  Sung-Jun Kim
Institution:1.Department of Biotechnology,Chosun University,Gwangju,Republic of Korea;2.BK21 Research Team for Protein Activity Control,Chosun University,Gwangju,Republic of Korea;3.Department of Alternative Medicine,Gwangju University,Gwangju,Republic of Korea;4.Department of Agro-Food Resources,National Academy of Agricultural Science, RDA,Suwon,Republic of Korea
Abstract:The present work was conducted to investigate the antioxidant activity and neuroprotective effects of Tripterygium regelii extract (TRE) on H2O2-induced apoptosis in human dopaminergic cells, SH-SY5Y. TRE possessed considerable amounts of phenolics (282.73 mg tannic acid equivalents/g of extract) and flavonoids (101.43 mg naringin equivalents/g of extract). IC50 values for reducing power and DPPH radical scavenging activity were 52.51 and 47.83 μg, respectively. The H2O2 scavenging capacity of TRE was found to be 57.68 μM × μg−1 min−1. By examining the effects of TRE on SH-SY5Y cells injured by H2O2, we found that after incubation of cells with TRE prior to H2O2 exposure, the H2O2 induced cytotoxicity was significantly reversed and the apoptotic features such as change in cellular morphology, nuclear condensation and DNA fragmentation was inhibited. Moreover, TRE was very effective attenuating the disruption of mitochondrial membrane potential and apoptotic cell death induced by H2O2. TRE extract effectively suppressed the up-regulation of Bax, Caspase-3 and -9, and down-regulation of Bcl-2. Moreover, TRE pretreatment evidently increased the tyrosine hydroxylase (TH) and brain-derived neurotrophic factor (BDNF) in SH-SY5Y cells. These findings demonstrate that TRE protects SH-SY5Y cells against H2O2-induced injury and antioxidant properties may account for its neuroprotective actions and suggest that TRE might potentially serve as an agent for prevention of neurodegenerative disease associated with oxidative stress.
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