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
AbstractSepsis-induced lung injury was the most common cause of death in patients. Topiroxostat, a novel xanthine oxidoreductase inhibitors, possessed obvious organ protectives effects. Xanthine oxidase played a vital role in acute lung injury. The study aimed to investigate the roles of Topiroxostat in sepsis-induced lung injury. The sepsis rats were established using cecum ligation and perforation. The lung damage induced by sepsis was evaluated by Hematoxylin and Eosin staining and lung tissue wet to dry ratio. The oxidative stress was detected by measurement of reactive oxygen species, malondialdehyde, myeloperoxidase and superoxide dismutase (SOD). The pro-inflammatory mediators, tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and monocyte chemotactic protein 1, were measured by Enzyme-Linked Immunosorbent Assay. The cell apoptosis in lung was detected by TUNNEL staining and western blot analysis of apoptosis-related proteins including pro-apoptosis proteins, Bax, cleaved caspase9, cleaved caspase3 and anti-apoptosis protein Bcl2. The results showed that Topiroxostat significantly reduced lung damage, along with decreased oxidative stress, inflammation response and apoptosis in sepsis rats. Topiroxostat exerted markedly protective effects in sepsis-induced lung injury and could be an antioxidant in treating sepsis-induced lung injury.
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