title: [Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats].
abstract: To investigate the influence of hydrogen sulfide (H₂S) on p38 MAPK signaling pathway during acute lung injury (ALI) caused by lipopolysaccharide (LPS), the rats were randomly divided into six groups: control group, LPS group, LPS + NaHS group, LPS + PPG (cystathionine-γ-lyase inhibitor) group, NaHS group and PPG group. The rats were sacrificed 6 h after injection and lung tissues were obtained. The structure of lung tissues and the number of polymorphonuclear leucocyte (PMN) was observed under optical microscope; the lung myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were tested; intercellular adhesion molecule-1 (ICAM-1) protein expression changes were detected by immunohistochemical staining; phosphorylated p38 MAPK (p-p38 MAPK) protein expression was detected by Western blotting. The results showed that the lung injury in LPS group was observed, at the same time the MPO activity, the content of MDA, ICAM-1 and p-p38 MAPK protein expressions, the number of PMN were all higher than those in control group (all P < 0.05). Pre-injection of NaHS alleviated the changes induced by LPS, while pre-injection of PPG aggravated those alterations (all P < 0.05). ICAM-1 and p-p38 MAPK protein expressions in lung tissue were positively correlated (r = 0.923, P < 0.01). The results suggest that H2S may reduce LPS-induced ALI through inhibiting the conjugation of p38 MAPK and reducing the expression of ICAM-1.
authors.affiliation: Departments of Ophthalmology, Physiology, Xingtai Medical College, China.
authors.forename: Ya-Min
authors.initials: YM
authors.lastname: Fan
authors.forename: Xin-Li
authors.initials: XL
authors.lastname: Huang
authors.forename: Ze-Fei
authors.initials: ZF
authors.lastname: Dong
authors.forename: Yi-Ling
authors.initials: YL
authors.lastname: Ling
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy*; D000818:Animals; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008070:Lipopolysaccharides; D008168:Lung / Q000378:metabolism / Q000473:pathology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D008315:Malondialdehyde / Q000494:pharmacology; D009504:Neutrophils; D009195:Peroxidase / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000494:pharmacology; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D009195:Peroxidase; D013482:Superoxide Dismutase; D048051:p38 Mitogen-Activated Protein Kinases; D006862:Hydrogen Sulfide