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: Ruhui Yang, Lina Yang, Xiangchun Shen, Wenyuan Cheng, Bohua Zhao, Kazi Hamid Ali, Zhiyu Qian, Hui Ji
• Journal: European journal of pharmacology (Eur J Pharmacol) Vol. 674 Issue 2-3 Pg. 391-6 (Jan 15 2012) ISSN: 1879-0712 [Electronic] Netherlands
• PMID: 21925167 (Publication Type: Journal Article)
• Copyright: Copyright © 2011 Elsevier B.V. All rights reserved.

Chemical References

• Ccl2 protein, mouse
• Chemokine CCL2
• Interleukin-6
• Lipopolysaccharides
• NF-kappa B
• Phosphoproteins
• Tumor Necrosis Factor-alpha
• trans-sodium crocetinate
• Vitamin A
• Carotenoids
• Peroxidase
• Superoxide Dismutase
• I-kappa B Kinase

Topics

• Acute Lung Injury (chemically induced, drug therapy, metabolism, pathology)
• Animals
• Carotenoids (pharmacology, therapeutic use)
• Chemokine CCL2 (genetics)
• Edema (chemically induced, drug therapy, metabolism, pathology)
• Female
• Gene Expression Regulation (drug effects)
• I-kappa B Kinase (metabolism)
• Interleukin-6 (genetics)
• Lipopolysaccharides (adverse effects)
• Male
• Mice
• Mice, Inbred ICR
• NF-kappa B (metabolism)
• Peroxidase (metabolism)
• Phosphoproteins (metabolism)
• Signal Transduction (drug effects)
• Superoxide Dismutase (metabolism)
• Tumor Necrosis Factor-alpha (genetics)
• Vitamin A (analogs & derivatives)