title: Insulin reduces LPS-induced lethality and lung injury in rats.
abstract: Insulin is a main glucose homeostatic hormone in the body. Previous reports showed that insulin also exerted anti-inflammatory actions and attenuated systemic inflammatory response. Here, we observed the effects and the underlying mechanisms of insulin on lipopolysaccharide (LPS)-induced acute lung injury (ALI). As revealed by survival study, insulin reduced mortality of rats and prolonged their survival time. Meanwhile, insulin significantly reduced the levels of inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and high mobility group box 1 (HMGB1) in bronchoalveolar lavage fluid (BALF). Besides, insulin markedly inhibited the expression of toll-like receptor 2 (TLR2), toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB). Taken together, these data provided information that insulin attenuated LPS-induced ALI may attribute partly to the inhibition of the production of cytokines, and the expression of TLR2, TLR4 and NF-κB.
authors.affiliation: Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi'an 710032, PR China.
authors.forename: Man-Ling
authors.initials: ML
authors.lastname: Liu
authors.forename: Hai-Ying
authors.initials: HY
authors.lastname: Dong
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Wan-Song
authors.initials: WS
authors.lastname: Zheng
authors.forename: Peng-Tao
authors.initials: PT
authors.lastname: Zhao
authors.forename: Yi
authors.initials: Y
authors.lastname: Liu
authors.forename: Wen
authors.initials: W
authors.lastname: Niu
authors.forename: Dun-Quan
authors.initials: DQ
authors.lastname: Xu
authors.forename: Zhi-Chao
authors.initials: ZC
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid; D016207:Cytokines / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology; D007328:Insulin / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D016328:NF-kappa B / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015996:Survival Rate; D051195:Toll-Like Receptor 2 / Q000235:genetics; D051197:Toll-Like Receptor 4 / Q000235:genetics
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D007328:Insulin; D008070:Lipopolysaccharides; D016328:NF-kappa B; C495343:Tlr2 protein, rat; C495347:Tlr4 protein, rat; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4