Myricetin attenuates lung inflammation and provides protection against lipopolysaccharide-induced acute lung injury by inhibition of NF-κB pathway in rats

Purpose: To investigate whether myricetin ameliorates lipopolysaccharide (LPS)-induced acute lung inflammation (ALI) in a rat model, and to elucidate the probable molecular mechanism of action involved. Methods: Myricetin (10, 20 and 40 mg/kg) was administered to rats 30 min after intratracheally administering LPS (5 mg/kg). BALF protein concentration, lung wet-to-dry weight ratio, myeloperoxidase (MPO) activity, cytokine production and migration of inflammatory cells were evaluated. Results: Myricetin significantly (p <= 0.05) attenuated lung inflammation as evident from the decreased wet-to-dry weight ratio of lungs, concentration of protein in the BALF, activity of MPO, cytokine production, and inflammatory cell migration. A decrease was also seen in TLR4, MyD88 and NF-kappa B expression. Additionally, an elevated antioxidant enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) was observed in all the treatment groups. Conclusion: Myricetin provides protection against LPS-induced ALI. The underlying mechanisms of its anti-inflammatory action may include inhibition of NF-kappa B-mediated inflammatory responses.