Antioxidant N-acetylcysteine blocks nerve growth factor-induced H 2O2/ERK signaling in PC12 cells

Liang-Yo Yang; Wun Chang Ko; Chun-Mao Lin; Jia-Wei Lin; Jen Chine Wu; Chien Ju Lin; Huey Hwa Cheng; Chwen-Ming Shih

doi:10.1196/annals.1338.056

Antioxidant N-acetylcysteine blocks nerve growth factor-induced H ₂O₂/ERK signaling in PC12 cells

Liang-Yo Yang, Wun Chang Ko, Chun-Mao Lin, Jia-Wei Lin, Jen Chine Wu, Chien Ju Lin, Huey Hwa Cheng, Chwen-Ming Shih

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

We investigated whether H₂O₂, superoxide, and ERK participate in nerve growth factor (NGF)-induced signaling cascades and whether antioxidant N-acetylcysteine (NAC) regulates these NGF-induced responses. PC12 cells were cultured in medium containing NGF or vehicle with or without NAC pretreatment, and the intracellular H₂O₂ and superoxide levels and the amount of phosphorylated ERK were evaluated by flow cytometry and Western blotting, respectively. We found that NGF increased intracellular H₂O₂ concentration and activated ERK but failed to affect intracellular superoxide level. Moreover, NAC counteracted these NGF-induced responses. These findings demonstrate that NAC blocks the NGF-induced H ₂O₂/ERK signaling in PC12 cells.

Original language	English
Pages (from-to)	325-337
Number of pages	13
Journal	Annals of the New York Academy of Sciences
Volume	1042
DOIs	https://doi.org/10.1196/annals.1338.056
Publication status	Published - 2005

Keywords

Antioxidant
ERK
Hydrogen peroxide
N-acetylcysteine
NGF
PC12 cells
Reactive oxygen species

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)
History and Philosophy of Science

Access to Document

10.1196/annals.1338.056

Cite this

Antioxidant N-acetylcysteine blocks nerve growth factor-induced H ₂O₂/ERK signaling in PC12 cells. / Yang, Liang-Yo; Ko, Wun Chang; Lin, Chun-Mao ; Lin, Jia-Wei; Wu, Jen Chine; Lin, Chien Ju; Cheng, Huey Hwa; Shih, Chwen-Ming.

In: Annals of the New York Academy of Sciences, Vol. 1042, 2005, p. 325-337.

Research output: Contribution to journal › Article › peer-review

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