Ameliorative effect of gossypin against acute lung injury in experimental sepsis model of rats

Aims: Sepsis is a complex pathophysiological event involving systemic inflammatory response syndrome, multiple organ dysfunction syndrome and tissue damage such as acute lung injury (ALI). Although many new mechanisms are being investigated to enlighten the pathophysiology of sepsis, there is no effective treatment protocol yet. Antioxidant, antibacterial and antiinflammatory effects of gossypin (GOS)-like flavonoids have been shown and we have hypothesized that GOS have roles in sepsis induced inflammation of lungs. Main methods: Cecal ligation and puncture (CLP) induced sepsis model was induced in rats. Effects of GOS on oxidative stress, histopathology, nuclear factor kappa B (NF-kappa B), IL-6 positivity and NLRP3, HMG beta 1, TNF-alpha, NF-kappa B, IL-1 beta mRNA expression levels were evaluated in lung tissues of the septic rats. Key findings: GOS 20 (20 mg/kg) administration to septic rats decreased oxidative stress and supported antioxidant system in lungs. GOS administration also decreased the tissue NF-kappa B and IL-6 immunopositivity, which is high in septic rats; and decreased the sepsis-induced lung injury. HMG beta 1, NLRP3, NF-kappa B, IL-1 beta, and TNF-alpha mRNA expression significantly increased in the CLP group. Both doses of GOS significantly reduced these mRNA expression as compared with the levels in the CLP group demonstrating its anti-inflammatory potential. Significance: GOS administration, may represent a novel treatment for the prevention of lung damage occurred after sepsis induction. This effect of GOS might be related to its anti-inflammatory potential that result in decreased cytokine response and improved oxidative status.