Forsythiaside Protects Against Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis in PC12 Cell
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- 作者：ChunKang Huang (1)
Yonglian Lin (2)
Hong Su (1)
Dongqing Ye (1)
1. School of Public Health ; Anhui Medical University ; 81 Meishan Rd. ; Hefei ; 230032 ; Anhui Province ; China
2. Fujian University of TCM ; 1 Qiuyang Rd. ; Fuzhou ; 350122 ; Fujian Province ; China - 关键词：Forsythiaside ; Neurodegenerative disorders ; Oxidative stress ; Apoptosis
- 刊名：Neurochemical Research
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：40
- 期：1
- 页码：27-35
- 全文大小：2,852 KB
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- 刊物主题：Biomedicine
Neurosciences
Biochemistry
Neurology - 出版者：Springer Netherlands
- ISSN：1573-6903
文摘
Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. We sought to elucidate possible effects of forsythiaside, an active constituent isolated from the Chinese medicinal herb Forsythia suspense, on hydrogen peroxide (H2O2)-induced cell death and to determine the underlying molecular mechanisms in neuron-like PC12 cells. We found that forsythiaside treatment effectively protected PC12 cells against H2O2-induced cell damage and apoptosis. H2O2 exposure induced oxidative stress in PC12 cells, as revealed by increased ROS and lipid peroxidation (MDA), which were inhibited by forsythiaside pretreatment. Increased Bax/Bcl-2 ratio, mitochondrial membrane potential decrease, cytochrome c release, caspase-9/-3 activation, AIF/Endo G translocation were observed in H2O2-treated cells. Interestingly, forsythiaside effectively prevented these events. These results suggested that forsythiaside prevented H2O2-induced mitochondria-dependent apoptosis. Further, increased nuclear levels of Nrf2 and up-regulation of antioxidant enzymes (Mn/SOD and CAT) were detected in forsythiaside-treated cells, indicating the anti-oxidative effects of forsythiaside might be associated with activation of Nrf2 pathway. Moreover, forsythiaside was proved to be effective to prevent LPS-induced cell death and ROS generation. In conclusion, forsythiaside effectively inhibited H2O2-induced oxidative stress and subsequent apoptosis activation.