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  • N-acetyl cysteine improves the effects of corticosteroids in a mouse model of chlorine-induced acute lung injury.

N-acetyl cysteine improves the effects of corticosteroids in a mouse model of chlorine-induced acute lung injury.

Toxicology (2014-12-17)
Elisabeth Wigenstam, Bo Koch, Anders Bucht, Sofia Jonasson
ABSTRACT

Chlorine (Cl2) causes tissue damage and a neutrophilic inflammatory response in the airways manifested by pronounced airway hyperreactivity (AHR). The importance of early anti-inflammatory treatment has previously been addressed. In the previous study, both high-dose and low-dose of dexamethasone (DEX) decreased the risk of developing delayed effects, such as persistent lung injuries, while only high-dose treatment could significantly counteract acute-phase effects. One aim of this study was to evaluate whether a low-dose of DEX in combination with the antioxidant N-acetyl cysteine (NAC) and if different treatments (Triptolide, Reparixin and Rolipram) administered 1h after Cl2-exposure could improve protection against acute lung injury in Cl2-exposed mice. BALB/c mice were exposed to 300 ppm Cl2 during 15 min. Assessment of AHR and inflammatory cells in bronchoalveolar lavage was analyzed 24h post exposure. Neither of DEX nor NAC reduced the AHR and displayed only minor effects on inflammatory cell influx when given as separate treatments. When given in combination, a protective effect on AHR and a significant reduction in inflammatory cells (neutrophils) was observed. Neither of triptolide, Reparixin nor Rolipram had an effect on AHR but Triptolide had major effect on the inflammatory cell influx. Treatments did not reduce the concentration of either fibrinogen or plasminogen activator inhibitor-1 in serum, thereby supporting the theory that the inflammatory response is not solely limited to the lung. These results provide a foundation for future studies aimed at identifying new concepts for treatment of chemical-induced lung injury. Studies addressing combination of anti-inflammatory and antioxidant treatment are highly motivated.

MATERIALS
Product Number
Brand
Product Description

Dexamethasone for peak identification, European Pharmacopoeia (EP) Reference Standard
Acetylcysteine, European Pharmacopoeia (EP) Reference Standard
Sigma-Aldrich
Triptolide, from Tripterygium wilfordii, ≥98% (HPLC), solid
Sigma-Aldrich
Dexamethasone 21-phosphate disodium salt, ≥98%
Sigma-Aldrich
Amyloid Protein Non-Aβ Component, ≥80% (HPLC)
USP
Acetylcysteine, United States Pharmacopeia (USP) Reference Standard
Sigma-Aldrich
N-Acetyl-L-cysteine, SAJ special grade, 98.0-102.0%
Dexamethasone, European Pharmacopoeia (EP) Reference Standard
Dexamethasone sodium phosphate, European Pharmacopoeia (EP) Reference Standard
Supelco
N-Acetyl-L-cysteine, Pharmaceutical Secondary Standard; Certified Reference Material
Sigma-Aldrich
N-Acetyl-L-cysteine, Sigma Grade, ≥99% (TLC), powder
Sigma-Aldrich
N-Acetyl-L-cysteine, BioXtra, ≥99% (TLC)
Sigma-Aldrich
Dexamethasone, powder, BioReagent, suitable for cell culture, ≥97%
Sigma-Aldrich
Dexamethasone, ≥98% (HPLC), powder
Sigma-Aldrich
Dexamethasone, meets USP testing specifications
Sigma-Aldrich
Rolipram, solid, ≥98% (HPLC)
Sigma-Aldrich
N-Acetyl-L-cysteine, suitable for cell culture, BioReagent
Sigma-Aldrich
Dexamethasone, powder, γ-irradiated, BioXtra, suitable for cell culture, ≥80% (HPLC)
Sigma-Aldrich
Dexamethasone, tested according to Ph. Eur.
Supelco
Dexamethasone, VETRANAL®, analytical standard
Dexamethasone sodium phosphate for peak identification, European Pharmacopoeia (EP) Reference Standard
USP
Dexamethasone, United States Pharmacopeia (USP) Reference Standard
Dexamethasone, British Pharmacopoeia (BP) Assay Standard
Supelco
Dexamethasone, Pharmaceutical Secondary Standard; Certified Reference Material
Dexamethasone for system suitability, European Pharmacopoeia (EP) Reference Standard