Open AccessInhibitory effects of hydrogen sulphide on pulmonary fibrosis in smoking rats via attenuation of oxidative stress and inflammation
Author(s) -
Zhou Xiang,
An Guoyin,
Chen Jianchang
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12254
Subject(s) - oxidative stress , inflammation , pulmonary fibrosis , superoxide dismutase , fibrosis , reactive oxygen species , malondialdehyde , chemistry , medicine , lung , glutathione peroxidase , tumor necrosis factor alpha , pathology , immunology , endocrinology , biochemistry
Accumulating evidence has demonstrated that hydrogen sulphide ( H 2 S ) is involved in the pathogenesis of various respiratory diseases. In the present study, we established a rat model of passive smoking and investigated whether or not H 2 S has protective effects against pulmonary fibrosis induced by chronic cigarette smoke exposure. Rat lung tissues were stained with haematoxylin‐eosin and M asson's trichrome. The expression of type I collagen was detected by immunohistochemistry. Oxidative stress was evaluated by detecting serum levels of malondialdehyde, superoxide dismutase and glutathione peroxidase and measuring reactive oxygen species generation in lung tissue. Inflammation was assessed by measuring serum levels of inflammatory cytokines, including high‐sensitivity C‐reactive protein, tumour necrosis factor‐α, interleukin ( IL )‐1β and IL ‐6. The protein expression of Nrf2, NF ‐κB and phosphorylated mitogen‐activated protein kinases ( MAPK s) in the pulmonary tissue was determined by W estern blotting. Our findings indicated that administration of NaHS (a donor of H 2 S ) could protect against pulmonary fibrosis in the smoking rats. H 2 S was found to induce the nuclear accumulation of Nrf2 in lung tissue and consequently up‐regulate the expression of antioxidant genes HO ‐1 and Trx‐1 in the smoking rats. Moreover, H 2 S could also reduce cigarette smoking‐induced inflammation by inhibiting the phosphorylation of ERK 1/2, JNK and p38 MAPK s and negatively regulating NF ‐κB activation. In conclusion, our study suggests that H 2 S has protective effects against pulmonary fibrosis in the smoking rats by attenuating oxidative stress and inflammation.