Attenuation of LPS-Induced Lung Inflammation by Glucosamine in Rats

Abstract

Acute inflammation is often observed during acute lung injury (ALI) and acute respiratory distress syndrome. Glucosamine is known to act as an anti-inflammatory molecule. The effects of glucosamine on acute lung inflammation and its associated mechanisms remain unclear. The present study sought to address how glucosamine plays an anti-inflammatory role in acute lung inflammation in vivo and in vitro. Using the LPS intratracheal instillation-elicited rat lung inflammation model, we found that glucosamine attenuated pulmonary edema and polymorphonuclear leukocyte infiltration, as well as the production of TNF-α, IL-1β, cytokine-induced neutrophil chemoattractant (CINC)-1, macrophage inflammatory protein (MIP)-2, and nitric oxide (NO) in the bronchoalveolar lavage fluid (BALF) and in the cultured medium of BALF cells. The expression of TNF-α, IL-1β, IFN-γ, CINC-1, MIP-2, monocyte chemotactic protein-1, and inducible NO synthase (iNOS) in LPS-inflamed lung tissue was also suppressed by glucosamine. Using the rat alveolar epithelial cell line L2, we noted that the cytokine mixture (cytomix)-regulated production and mRNA expression of CINC-1 and MIP-2, NO production, the protein and mRNA expression of iNOS, iNOS mRNA stability, and iNOS promoter activity were all inhibited by glucosamine. Furthermore, glucosamine reduced LPS-mediated NF-κB signaling by decreasing IκB phosphorylation, p65 nuclear translocation, and NF-κB reporter activity. Overexpression of the p65 subunit restored the inhibitory action of glucosamine on cytomix-regulated NO production and iNOS expression. In conclusion, glucosamine appears to act as an anti-inflammatory molecule in LPS-induced lung inflammation, at least in part by targeting the NF-κB signaling pathway.

Pulmonary toxicity of well-dispersed titanium dioxide nanoparticles following intratracheal instillation

“…It has been reported that different expression patterns of the CINC family have been observed in various inflammation models. There was a high concentration of CINC-1 and CINC-2 in the airway of a rat model of chronic bronchopulmonary infection with Pseudomonas aeruginosa (Amano et al 2000 ), and Chuang et al reported that the protein and mRNA expression of CINC-1 was upregulated in an acute lung injury model induced by intratracheal LPS instillation (Chuang et al 2013 ). In the 1.0 mg-administered group in the present study, TiO 2 nanoparticles induced a transient expression of CINC in the rat lung after intratracheal instillation, but not in the 0.2 mg-administered group.…”

Glucosamine improves survival in a mouse model of sepsis and attenuates sepsis-induced lung injury and inflammation

“…Data from the current study have revealed a strong anti-inflammatory effect of GlcN in a sepsis model by attenuating pulmonary edema, neutrophil infiltration, nitrite production, and inflammatory cytokine production, as well as M1 polarization. GlcN is reported to attenuate LPS-induced lung inflammation in rats (30). The earlier study used intratracheal instillation of LPS to elicit local lung inflammation in rat and anti-inflammatory effects of GlcN in response to the cytokine mixture are examined using the rat alveolar cell line, L2.…”

Shufeng Jiedu Capsule protect against acute lung injury by suppressing the MAPK/NF-κB pathway

“…IL-1β and TNF-α may serve as biomarkers of the NF-κB inflammatory pathway. A previous study using DXMS as a positive control determined levels of IL-1β and TNF-α to assess the protective effect of SFJDC in a rat model of LPS-induced ALI (26). Confocal laser scanning imaging revealed an obvious decrease in the levels of IL-1β in both rats treated with SFJDC and rats treated with DXMS compared to rats with untreated ALI.…”