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.