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Oral N-acetylcysteine attenuates the rat pulmonary inflammatory response to antigen

Depts of ¹ Pharmacology and ⁴ Physiology, Faculty of Medicine, University of Valencia, and ² Dept of Medical Bioanalysis, Institute of Biomedical Research of Barcelona, Spanish Council for Scientific Research, Barcelona, Spain. ³ Zambon Group SpA, Bresso, Italy

CORRESPONDENCE: E.J. Morcillo, Dept of Pharmacology, Faculty of Medicine, 15 Av. Blasco Ibáñez, E-46010, Valencia, Spain. Fax: 34 963864622. E-mail: esteban.morcillo@uv.es

Keywords: N-Acetylcysteine, airway inflammation, experimental asthma, inducible nitric oxide synthase, nuclear transcription factor-B

Received: May 14, 2002
Accepted October 8, 2002

S. Blesa, M. Mata and A. Serrano were supported by the Ministry of Science and Technology (Madrid, Spain) and J. Suchankova by a North Atlantic Treaty Organisation (Brussels, Belgium) grant. This study was supported by grants from the European Union and Spanish Ministry of Science and Technology (1FD97-1143, SAF1999-0111 and SAF2000-0144) and a research grant from Zambon Group SpA (Bresso, Italy).

Oxidative stress is involved in the pathophysiology of inflammatory airway diseases including asthma; therefore, antioxidants might be of clinical benefit in asthma treatment. In the present study, the effects of N-acetylcysteine on sensitised brown Norway rats were examined.

N-Acetylcysteine (3 mmol·kg body weight^–1 administered orally) was given daily for 1 week before challenge and various antigen-induced pulmonary responses were studied.

Antigen exposure increased lipid peroxidation in bronchoalveolar lavage fluid (BALF) and oxidised glutathione levels in lung tissue 2 h after challenge. Lung nuclear transcription factor-B-binding activity was increased 2 h after challenge, and BALF tumour necrosis factor- and inducible nitric oxide synthase expression in lungs peaked 4 h after challenge. Expression of intercellular adhesion molecule-1 and mucin MUC5AC was also increased 4 h after challenge. These changes in oxidant status, transcription factor activation, and inflammatory cytokine and gene expression were reduced by N-acetylcysteine. This thiol did not affect the immediate bronchospasm reaction to antigen in anaesthetised rats but inhibited airways hyperresponsiveness to 5-hydroxytryptamine and the augmented eosinophil numbers in BALF, which appear 24 h after exposure of conscious rats to antigen aerosol, and abolished antigen-induced extravasation of Evans blue into BALF.

These results indicate that oral N-acetylcysteine exerts an antioxidant protective effect and attenuates pulmonary inflammation in experimental asthma.

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