title: Suppression of NF-κB pathway by crocetin contributes to attenuation of lipopolysaccharide-induced acute lung injury in mice.
abstract: Crocetin, a carotenoid compound, has been shown to reduce expression of inflammation and inhibit the production of reactive oxygen species. In the present study, the effect of crocetin on acute lung injury induced by lipopolysaccharide (LPS) was investigated in vivo. In the mouse model, pretreatment with crocetin at dosages of 50 and 100 mg/kg reduced the LPS-induced lung oedema and histological changes, increased LPS-impaired superoxide dismutase (SOD) activity, and decreased lung myeloperoxidase (MPO) activity. Furthermore, treatment with crocetin significantly attenuated LPS-induced mRNA and the protein expressions of interleukin-6 (IL-6), macrophage chemoattractant protein-1 (MCP-1), and tumour necrosis factor-α (TNF-α) in lung tissue. In addition, crocetin at different dosages reduced phospho-IκB expression and NF-κB activity in LPS-induced lung tissue alteration. These results indicate that crocetin can provide protection against LPS-induced acute lung injury in mice.
authors.affiliation: Department of pharmacology, China Pharmaceutical University, 24 Tongjia Xiang, Nanjing 210009, PR China.
authors.forename: Ruhui
authors.initials: R
authors.lastname: Yang
authors.forename: Lina
authors.initials: L
authors.lastname: Yang
authors.forename: Xiangchun
authors.initials: X
authors.lastname: Shen
authors.forename: Wenyuan
authors.initials: W
authors.lastname: Cheng
authors.forename: Bohua
authors.initials: B
authors.lastname: Zhao
authors.forename: Kazi Hamid
authors.initials: KH
authors.lastname: Ali
authors.forename: Zhiyu
authors.initials: Z
authors.lastname: Qian
authors.forename: Hui
authors.initials: H
authors.lastname: Ji
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D002338:Carotenoids / Q000494:pharmacology* / Q000627:therapeutic use; D018932:Chemokine CCL2 / Q000235:genetics; D004487:Edema / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D051550:I-kappa B Kinase / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics; D008070:Lipopolysaccharides / Q000009:adverse effects*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D010750:Phosphoproteins / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D014801:Vitamin A / Q000031:analogs & derivatives
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010750:Phosphoproteins; D014409:Tumor Necrosis Factor-alpha; C487773:trans-sodium crocetinate; D014801:Vitamin A; D002338:Carotenoids; D009195:Peroxidase; D013482:Superoxide Dismutase; D051550:I-kappa B Kinase