N-acetylcysteine attenuates subcutaneous administration of bleomycin-induced skin fibrosis and oxidative stress in a mouse model of scleroderma
Autor: | Jun-Feng Yu, Qi-Xing Zhu, Tao Jiang, Q.-Y. Yu, Cheng-Fan Zhou, S.-H. Xu, Jiaxiang Zhang |
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Rok vydání: | 2013 |
Předmět: |
congenital
hereditary and neonatal diseases and abnormalities Pathology medicine.medical_specialty Injections Subcutaneous Dermatology Pharmacology Bleomycin medicine.disease_cause Acetylcysteine Superoxide dismutase Lipid peroxidation Mice Scleroderma Localized chemistry.chemical_compound Fibrosis Malondialdehyde Animals Medicine Skin chemistry.chemical_classification Mice Inbred BALB C Reactive oxygen species Antibiotics Antineoplastic integumentary system biology Superoxide Dismutase business.industry nutritional and metabolic diseases Free Radical Scavengers Catalase Thiobarbiturates medicine.disease Disease Models Animal Oxidative Stress chemistry biology.protein Female Reactive Oxygen Species business Oxidative stress medicine.drug |
Zdroj: | Clinical and Experimental Dermatology. 38:403-409 |
ISSN: | 0307-6938 |
DOI: | 10.1111/ced.12033 |
Popis: | 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. |
Databáze: | OpenAIRE |
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