Conflict of interest: none declared.
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Experimental dermatology ● Original article
N-acetylcysteine attenuates subcutaneous administration of bleomycin-induced skin fibrosis and oxidative stress in a mouse model of scleroderma
Article first published online: 21 MAR 2013
DOI: 10.1111/ced.12033
© The Author(s) CED © 2013 British Association of Dermatologists
Additional Information
How to Cite
Zhou, C.-F., Yu, J.-F., Zhang, J.-X., Jiang, T., Xu, S.-H., Yu, Q.-Y. and Zhu, Q.-X. (2013), N-acetylcysteine attenuates subcutaneous administration of bleomycin-induced skin fibrosis and oxidative stress in a mouse model of scleroderma. Clinical and Experimental Dermatology, 38: 403–409. doi: 10.1111/ced.12033
Publication History
- Issue published online: 23 APR 2013
- Article first published online: 21 MAR 2013
- Manuscript Accepted: 22 JUL 2012
Funded by
- grants from the College young talents Foundation of Anhui province. Grant Number: 2010SQRL071ZD
- Natural Science Foundation of Anhui province. Grant Number: 1208085QH170
- Abstract
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Summary
Background
Several lines of evidence suggest that the generation of reactive oxygen species (ROS) is of major importance in the pathogenesis of scleroderma, and thus antioxidant therapy may be useful for patients with an impaired oxidative defence mechanism.
Aim
To examine the effect of N-acetylcysteine (NAC) on skin fibrosis and oxidative stress in a bleomycin (BLM)-induced mouse model of scleroderma.
Methods
We used this mouse model to evaluate the effect of NAC on skin fibrosis and oxidative stress. Skin fibrosis was evaluated by histopathological examination and hydroxyproline content. To measure lipid peroxidation, we used a thiobarbituric acid-reactive species, malondialdehyde (MDA). Oxidative protein damage (carbonyl content) and the activities of catalase (CAT) and superoxide dismutase (SOD) were determined to evaluate oxidative stress in the skin tissue.
Results
Treatment with NAC attenuated the skin fibrosis induced by BLM, significantly reducing the MDA and protein carbonyl content in these mice. SOD activity in BLM-only mice and BLM plus NAC-treated mice was increased compared with control mice. However, there was no significant difference in skin SOD activity of mice treated with both BLM and NAC compared with those treated with BLM only. In addition, CAT activity was not altered in the BLM plus NAC mice.
Conclusions
NAC treatment attenuates skin fibrosis in a BLM-induced mouse model of scleroderma, and this is associated with diminished oxidative stress. The results suggest that NAC may be a potential therapeutic agent for patients with scleroderma.
