title: Leptin attenuates lipopolysaccharide or oleic acid-induced acute lung injury in mice.
abstract: Leptin is reported to be involved in acute lung injury (ALI). However, the role and underlying mechanisms of leptin in ALI remain unclear. The aim of this study was to determine whether leptin deficiency promoted the development of ALI. LPS or oleic acid (OA) were administered to wild-type and leptin deficient (ob/ob) mice to induce ALI. Leptin level, survival rate, and lung injury were examined. Results showed that leptin levels were predominantly increased in the lung, but also in the heart, liver, kidney, and adipose tissue after LPS adminiatration. Compared with wild-type mice, LPS- or OA-induced lung injury was worse and the survival rate was lower in ob/ob mice. Moreover, leptin deficiency promoted the release of proinflammatory cytokines. Exogenous administration of leptin reduced lethality in ob/ob mice and ameliorated lung injury partly through inhibiting the activation of NF-κB, p38, and ERK pathways. These results indicated that leptin deficiency contributed to the development of lung injury by enhancing inflammatory response, and a high level of leptin improved survival and protected against ALI.
authors.affiliation: 1 Department of Pathology, Xijing Hospital.
authors.forename: Hai-Ying
authors.initials: HY
authors.lastname: Dong
authors.forename: Min
authors.initials: M
authors.lastname: Xu
authors.forename: Zhen-Yu
authors.initials: ZY
authors.lastname: Ji
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Wang
authors.forename: Ming-Qing
authors.initials: MQ
authors.lastname: Dong
authors.forename: Man-Ling
authors.initials: ML
authors.lastname: Liu
authors.forename: Dun-Quan
authors.initials: DQ
authors.lastname: Xu
authors.forename: Peng-Tao
authors.initials: PT
authors.lastname: Zhao
authors.forename: Yi
authors.initials: Y
authors.lastname: Liu
authors.forename: Ying
authors.initials: Y
authors.lastname: Luo
authors.forename: Wen
authors.initials: W
authors.lastname: Niu
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Ye
authors.forename: Zhi-Chao
authors.initials: ZC
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism; D020738:Leptin / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D016328:NF-kappa B / Q000378:metabolism; D019301:Oleic Acid / Q000633:toxicity*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D020738:Leptin; D008070:Lipopolysaccharides; D016328:NF-kappa B; D019301:Oleic Acid