Neuroprotective effect of N-acetylcysteine on neuronal apoptosis induced by a synthetic gingerdione compound: Involvement of ERK and p38 phosphorylation

Chia Ho Lin, Sheng Chu Kuo, Li Jiau Huang, Po-Wu Gean

研究成果: Article同行評審

19 引文 斯高帕斯(Scopus)

摘要

Besides being used as a spice, ginger has been applied in oriental medicine to ameliorate symptoms such as inflammatory, rheumatic disorders, and gastrointestinal discomforts. The effects of ginger on neuronal cells, however, have not been explored. We investigate the effect of 1-(3,4-dimethoxyphenyl)-3, 5-dodecenedione (I6), a derivative of gingerdione, on cultured cortical neurons. After a 5-day maturation period in vitro, cortical neurons were treated with I6 for 24 hr and cell viability was assessed using MTT assay. I6 induced neuronal death in a concentration-dependent manner. Hoechst 33342, propidium iodide (PI), and TUNEL staining confirmed that the reduced cell viability by I6 was due to apoptosis. Pre-treatment of cell with N-acetylcysteine (NAC) prevented cell death in a concentration-dependent manner. N-acetylcysteine increased phosphorylated levels of p42 and p44 extracellular signal-regulated kinases (ERKs). In parallel, farnesyltransferase and MEK inhibitors blocked ERK phosphorylation and neuroprotective effect of NAC. Unexpectedly, NAC also increased phosphorylated level of p38 mitogen-activated protein kinase (MAPK) and p38 specific inhibitors dose-dependently attenuated the effect of NAC. Farnesyltransferase and MEK inhibitors completely abolished NAC-induced p38 phosphorylation whereas p38 inhibitor did not influence NAC-induced ERK phosphorylation. These results show that NAC serially activates ERKs and p38 MAPK, and ERKs and p38 work together to mediate the neuroprotective effect Of NAC.

原文English
頁(從 - 到)1485-1494
頁數10
期刊Journal of Neuroscience Research
84
發行號7
DOIs
出版狀態Published - 2006 十一月 15

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

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