Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (7): 1159-1164.doi: 10.4103/1673-5374.187057

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Protective effects of ginsenoside Rg1 against hydrogen peroxide-induced injury in human neuroblastoma cells

Zhi-gao Sun1, Li-ping Chen2, *, Fa-wei Wang2, Cheng-yong Xu1, Miao Geng3   

  1. 1 Department of Traditional Chinese Medicine, Hainan Branch Hospital of Chinese PLA General Hospital, Sanya, Hainan Province, China 2 Department of Traditional Chinese Medicine, Chinese PLA General Hospital, Beijing, China 3 Institute of Gerontology, Chinese PLA General Hospital, Beijing, China
  • Online:2016-07-30 Published:2016-07-30
  • Contact: Li-ping Chen, M.D., lipingschen@aliyun.com.
  • Supported by:
    This research was supported by the Research and Development Project Fund of Science and Technology Plan Program of Science and Technology Bureau of Beijing of China, No. Z111107067311022.

Abstract: The active ingredient of ginseng, ginsenosides Rg1, has been shown to scavenge free radicals and improve antioxidant capacity. This study hypothesized that ginsenosides Rg1 has a protective role in human neuroblastoma cells injured by H2O2. Ginsenosides Rg1 at different concentrations (50 and 100 μM) was used to treat H2O2 (150 μM)-injured SH-SY5Y cells. Results demonstrated that ginsenoside Rg1 elevated the survival rate of SH-SY5Y cells injured by H2O2, diminished the amount of leaked lactate dehydrogenase, and increased superoxide dismutase activity. Ginsenoside Rg1 effectively suppressed caspase-3 immunoreactivity, and contributed to heat shock protein 70 gene expression, in a dose-dependent manner. These results indicate that ginsenoside Rg1 has protective effects on SH-SY5Y cells injured by H2O2 and that its mechanism of action is associated with anti-oxidation and the inhibition of apoptosis.

Key words: nerve regeneration, traditional Chinese medicine monomer, ginsenoside Rg1, SH-SY5Y cells, H2O2, cerebral ischemia, cell apoptosis, lactate dehydrogenase, superoxide dismutase, caspase-3, heat shock protein 70, dose-effect relationship, neural regeneration