title: Ghrelin attenuates sepsis-associated acute lung injury oxidative stress in rats.
abstract: This study investigated the effect of ghrelin on oxidative stress in septic rat lung tissue. Male Sprague-Dawley rats were divided into sham-operation, sepsis, and ghrelin groups. Sepsis was induced by cecal ligation and puncture. Ghrelin was administered intraperitoneally at 3 and 15 h post-operation. Bronchoalveolar lavage was performed to collect alveolar macrophages (AMs). Inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) expression in alveolar macrophages and iNOS protein levels were measured by reverse transcription PCR (RT-PCR) and Western blot. Pulmonary pathology was analyzed and nitrotyrosine expression was examined by immunohistochemistry. Plasma superoxide dismutase (SOD) and lung wet/dry weight were measured. In the sepsis group, iNOS mRNA expression in AMs was 1.33 ± 0.05, 1.44 ± 0.08, and 1.57 ± 0.11 at 6, 12, and 20 h post-surgery, respectively, and were higher compared with the sham-operation group (p<0.05). No increase was observed at longer time points. iNOS mRNA expression in the sepsis group was lower compared with the ghrelin group (2.27 ± 0.37) (p<0.05) at 20 h post-surgery. iNOS protein levels in the ghrelin group (0.87 ± 0.03, p<0.05) were lower than in the sepsis group at 20 h. Ghrelin group pathological scores were lower than in the sepsis group (p<0.05). Plasma SOD was slightly non-significantly decreased in the ghrelin group. No difference was observed in lung wet/dry weight ratios between sepsis and ghrelin groups. iNOS mRNA expression in AMs was elevated between 6 and 20 h after cecal ligation and puncture (CLP), but did not progress. Ghrelin attenuated pulmonary iNOS protein expression and tended to increase plasma SOD activity. Ghrelin suppressed pulmonary nitrosative stress in septic rats, but did not improve lung wet/dry weight ratios.
authors.affiliation: Department of Medical Intensive Care Unit, First Affiliated Hospital of Sun Yat-sen University, 58 2nd Zhongshan Road, Guangzhou, GuangDong, 510080, People's Republic of China, zengmian2004@163.com.
authors.forename: Mian
authors.initials: M
authors.lastname: Zeng
authors.forename: Wanmei
authors.initials: W
authors.lastname: He
authors.forename: Lijun
authors.initials: L
authors.lastname: Li
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Liang
authors.initials: L
authors.lastname: Luo
authors.forename: Xubin
authors.initials: X
authors.lastname: Huang
authors.forename: Kaipan
authors.initials: K
authors.lastname: Guan
authors.forename: Weiling
authors.initials: W
authors.lastname: Chen
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D054439:Ghrelin / Q000494:pharmacology / Q000627:therapeutic use*; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D054439:Ghrelin