Luteolin attenuates the pulmonary inflammatory response involves abilities of antioxidation and inhibition of MAPK and NFκB pathways in mice with endotoxin-induced acute lung injury

摘要: Acute lung injury (ALI) in critically ill patients remains the leading cause of mortality and morbidity. Lipopolysaccharide (LPS) is a key mediator injury. This study investigates protective effects mechanisms luteolin intratracheal instillation LPS (100μg)-induced ALI mice. Pretreatment mice with 70μmol/kg significantly restores LPS-induced decrease oxygen pressure increase carbon dioxide arterial blood. The histopathological established pretreatment markedly attenuates changes, such as haemorrhaging, interstitial edema, infiltration polymorphonuclear neutrophils (PMNs) into parenchyma alveolar spaces. Sufficient evidence for (35 70μmol/kg) suppresses activation PMNs obtained expression surface marker CD11b Ly6G on cells bronchoalveolar lavage fluid (BALF) myeloperoxidase activity tissue. Furthermore, reduces catalase superoxide dismutase, level oxidative damage, lipid peroxidation, In addition, secretion TNF-α, KC, ICAM-1 BALF after challenge are also inhibited by luteolin. Moreover, reduced MAPK NFκB pathways. Therefore, potential antagonists