Effect of Taxifolin on Lung Injury Induced by Staphylococcus aureus in Albino Wistar-Type Rats: A Biochemical and Histopathological Evaluation

Background and Objective: Staphylococcus aureus is considered the main cause of pneumonia. Pneumonia is the most common cause of acute lung injury. Taxifolin is a flavonol with antioxidant, anti-inflammatory, antimicrobial, antiviral, antifungal, anti-hyperglycemic, anti-hyperlipidemic, anti-psoriatic and pulmono-protective activities. The present study aimed to biochemically and histopathologically investigate the protective effect of taxifolin against possible acute lung oxidative and inflammatory damage caused by Staphylococcus aureus ( S. aureus) infection in rats. Materials and Methods: The rats were divided into three groups 6 rats each, healthy control (HG), S. aureus inoculated (SaG) and S. aureus inoculated+taxifolin treated (SaT). Animals were euthanized. Malondialdehyde (MDA) total glutathione (tGSH), Nuclear Factor kappa B (NF-kappa B), Tumor Necrosis Factor-alpha (TNF-alpha) and Interleukin One Beta (IL-1 beta) levels were measured in the excised lung tissues and also examined histopathologically. Results: S. aureus inoculation significantly increased MDA, NF-kappa B, TNF-alpha and IL-1 beta levels and decreased tGSH levels in lung tissue. Treatment with taxifolin significantly suppressed the increase in MDA, NF-kappa B, TNF-alpha and IL-1 beta levels and the decrease in tGSH levels. Histopathologically, S. aureus inoculation led to severe mononuclear cell infiltration in interstitial areas, lymphoid hyperplasia in bronchial-associated lymphoid tissue and desquamation in bronchial epithelium. Treatment with taxifolin attenuated these histopathological findings. Conclusion: Current experimental results suggested that taxifolin may be beneficial in the treatment of oxidative and inflammatory lung injury associated with S. aureus infection.