Antioxidant Activity and Protective Effects of Tripterygium regelii Extract on Hydrogen Peroxide-Induced Injury in Human Dopaminergic Cells, SH-SY5Y

• Published in: Neurochemical research 2010-08, Vol.35 (8), p.1269-1280
• Main Authors: Choi, Bong-Suk, Sapkota, Kumar, Kim, Seung, Lee, Hyo Jeong, Choi, Han-Seok, Kim, Sung-Jun
• Format: Article
• Language: English
• Subjects: Antioxidants - pharmacology; Apoptosis - drug effects; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain-Derived Neurotrophic Factor - biosynthesis; Caspase 3 - metabolism; Caspase 9 - metabolism; Cell Biology; Cell Line; Dopamine - metabolism; Enzyme Activation; Flavonoids - pharmacology; Free Radical Scavengers - pharmacology; Humans; Hydrogen Peroxide - pharmacology; Membrane Potential, Mitochondrial - drug effects; Neurochemistry; Neurology; Neuroprotective Agents - pharmacology; Neurosciences; Original Paper; Phenols - pharmacology; Plant Extracts - chemistry; Plant Extracts - pharmacology; Proto-Oncogene Proteins c-bcl-2 - biosynthesis; Tripterygium; Tyrosine 3-Monooxygenase - biosynthesis
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-010-0185-4

The present work was conducted to investigate the antioxidant activity and neuroprotective effects of Tripterygium regelii extract (TRE) on H 2 O 2 -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). IC 50 values for reducing power and DPPH radical scavenging activity were 52.51 and 47.83 μg, respectively. The H 2 O 2 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 H 2 O 2 , we found that after incubation of cells with TRE prior to H 2 O 2 exposure, the H 2 O 2 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 H 2 O 2 . 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 H 2 O 2 -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.