Acylated catalpol diglycoside ameliorates lipopolysaccharides-induced acute lung injury through inhibition of iNOS and TNF-α expression.

Acute lung injury (ALI) is a universal cause of respiratory failure and death especially after sepsis. The current study evaluates the protective efficacy of acylated catalpol diglycoside (ACD), a plant iridoid glycoside, against lipopolysaccharides (LPS)-induced ALI in rats. ACD prevented LPS-induced elevations in total and differential cell counts and total protein content in bronchoalveolar lavage fluid, lung malondialdehyde content, and serum lactate dehydrogenase activity. Moreover, ACD significantly increased lung glutathione and superoxide dismutase and improved lung histopathology with significant reduction in lung tumor necrosis factor-α (TNF-α) content mediated mainly via inhibition of TNF-α messenger RNA (mRNA) expression. In addition, ACD significantly reduced lung total nitrate concentration content through downregulation of inducible nitric oxide synthase (iNOS) mRNA expression, negating the excessive undesired vasodilatation characteristic to sepsis. In conclusion, the reduction of oxidative stress, amelioration of inflammatory cytokines expression, and antagonism of sepsis associated-excessive vasodilatation are main contributors in ACD's protective effect in LPS-induced ALI in rats.