Protective effect of arctigenin on ethanol-induced neurotoxicity in PC12 cells
Autor: | Jia Huang, Jing‑Xiang Wei, Lan Xiao, Yong‑Tang Wang, Ya‑Hai Shu, Shi‑Qi Fang, Xiu‑Min Lu |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Cancer Research Cell Survival Apoptosis Biology PC12 Cells Biochemistry Neuroprotection Lignans 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Neurotrophic factors Genetics medicine Animals Propidium iodide Furans Molecular Biology Cell damage Arctigenin Cell Proliferation Neurons Ethanol Cell Cycle Neurotoxicity Cell cycle medicine.disease Arctium Rats Cell biology Neuroprotective Agents 030104 developmental biology Oncology chemistry Molecular Medicine 030217 neurology & neurosurgery |
Zdroj: | Molecular Medicine Reports. 15:2235-2240 |
ISSN: | 1791-3004 1791-2997 |
DOI: | 10.3892/mmr.2017.6222 |
Popis: | As a neurotropic substance, ethanol can damage nerve cells through an increase in the production of free radicals, interference of neurotrophic factor signaling pathways, activation of endogenous apoptotic signals and other molecular mechanisms. Previous studies have revealed that a number of natural drugs extracted from plants offer protection of nerve cells from damage. Among these, arctigenin (ATG) is a lignine extracted from Arctium lappa (L.), which has been found to exert a neuroprotective effect on scopolamine‑induced memory deficits in mice with Alzheimer's disease and glutamate-induced neurotoxicity in primary neurons. As a result, it may offer beneficial effects on ethanol-induced neurotoxicity. However, the effects of ATG on ethanol‑induced nerve damage remain to be elucidated. To address this issue, the present study used rat pheochromocytoma PC12 cells to investigate the neuroprotective effects of ATG on ethanol-induced cell damage by performing an MTT reduction assay, cell cycle analysis, Hoechst33342/propidium iodide fluorescence staining and flow cytometry to examine apoptosis. The results showed that 10 µM ATG effectively promoted the proliferation of damaged cells, and increased the distribution ratio of the cells at the G2/M and S phases (P |
Databáze: | OpenAIRE |
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