Effects of N-acetylcysteine on oxidative stress in lung
tissue of smoked rats

doi:10.3969/j.issn.2095-4344.1877

Abstract

Abstract:

BACKGROUND: N-Acetyl-L-cysteine is a precursor of glutathione, which can directly scavenge oxygen free radicals. However, it is not entirely clear whether N-acetyl-L-cysteine can alleviate smoking-induced lung injury by reducing oxidative stress.

OBJECTIVE: To investigate the effects of N-acetylcysteine on oxidative stress in lung tissue of smoked rats, and to clarify its possible mechanism of action.

METHODS: Thirty male rats were randomly divided into control, smoked and smoked+N-acetylcysteine groups. The rats in the smoked and smoked+N-acetylcysteine groups were placed in the passive smoking animal exposure system, with smoking of 20 cigarettes, twice/d, 1 hour/times, for 8 consecutive weeks. The rats in the smoked+N-acetylcysteine group were given 200 mg/kg N-acetylcysteine via gavage before passive smoking daily, for 8 consecutive weeks. The control rats were fed normally for 8 consecutive weeks. The study was approved by the Laboratory Animal Ethical Committee of Shenyang Medical College in October 2018, approval No. (2018)85.

RESULTS AND CONCLUSION: (1) Pathological observation showed that the pulmonary tissue was disordered, alveolar septal thickening, inflammatory cell infiltration and interstitial fibrosis in the smoking group, while the pulmonary hemorrhage, the number of inflammatory cells and the degree of fibrosis in the smoking+N-acetylcysteine group were significantly reduced. (2) Compared with the control group, the expression levels of malondialdehyde-5 and inositol-alpha genes were significantly increased, and superoxide dismutase-1 gene expression was significantly decreased in the smoked group, while N-acetylcysteine could inhibit the above changes. (3) Immunofluorescence staining and western blot assay results revealed that the expression levels of malondialdehyde-5 and inositol-alpha in lung tissue of rats in the smoked+N-acetylcysteine group was significantly lower than those in the smoked group, and the expression level of superoxide dismutase-1 was significantly higher than that in the smoked group. In addition, the expression levels of Nrf2 and Keap1 mRNA and protein were significantly increased, and the expression levels of Bach1 mRNA and protein were significantly decreased in the smoking+N-acetylcysteine group. (4) These results suggest that N-acetylcysteine can protect smoking-induced lung injury by reducing oxidative stress, and which might be through activating Nrf2/Keap1 signaling pathway.

Key words: smoked, N-acetylcysteine, homocysteine, oxidative stress, Nrf2/Keap1 signaling pathway, lung injury, malondialdehyde-5, inositol-alpha

CLC Number:

R453.9

TS41+3

R563

Li Xiang, Wang Wei, Xia Shuyue, He Wei. Effects of N-acetylcysteine on oxidative stress in lung tissue of smoked rats[J]. Chinese Journal of Tissue Engineering Research, 2020, 24(2): 254-259.

Figures/Tables 6

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