Potential effect of astragaloside IV on the lipopolysaccharide induced inflammation via the inactivation of NF-κB signaling pathway

Background: The host treats lipopolysaccharides (LPS) as a sign of microbial invasion by pathogenic Gram-negative bacteria. In lungs, LPS activates a cascade of inflammatory reactions leading to inflammation. Previous investigation suggests that astragaloside IV (AG) has an anti-inflammatory and antioxidant effect, but the potential mechanism of lung inflammation is still unknown. In this experimental study, we aimed to investigate the anti-inflammatory potential of AG against LPS-induced lung inflammation. Materials and Methods: In this study, we used Sprague Dawley rats for the experimental protocol. Animals were injected with LPS (10 mg/kg, b. w.) for the induction of lung inflammation and were subsequently administered with AG (1.25, 2.5, and 5 mg/kg). At the end of the experiment, acute phase response and lipid parameters were estimated. Pro-inflammatory cytokines and inflammatory mediators were also estimated. Furthermore, quantitative real-time polymerase chain reaction was used to estimate the inflammatory markers and expression of mRNA of apoptosis markers. Results: AG treatment significantly increased the survival rate as compared to LPS control. AG significantly (P < 0.001) altered the renal, hepatic, lipid, and antioxidant parameter at dose dependent manner. AG significantly (P < 0.001) decreased the level of malondialdehyde and reduced glutathione and increased he activity of superoxide dismutase. AG significantly (P < 0.001) decreased the level of nuclear factor kappa B (NF-κB). In addition, AG significantly (P < 0.001) down-regulated the expression of inflammatory cytokines such as interleukin (IL)-1, IL-6, IL-1 β, tumor necrosis factor-α, IL-18 and upregulated the expression of IL-4 and IL-10. Conclusion: In summary, these findings indicate that AG effectively suppressed the LPS-induced inflammation through inactivation of NF-κB signaling pathway.