Arctigenin Protects against Lipopolysaccharide-Induced Pulmonary Oxidative Stress and Inflammation in a Mouse Model via Suppression of MAPK, HO-1, and iNOS Signaling

• Published in: Inflammation 2015-08, Vol.38 (4), p.1406-1414
• Main Authors: Zhang, Wen-zhou, Jiang, Zheng-kui, He, Bao-xia, Liu, Xian-ben
• Format: Article
• Language: English
• Subjects: Acute Lung Injury - metabolism; Acute Lung Injury - prevention & control; Animals; Arctium lappa; Biomedical and Life Sciences; Biomedicine; Disease Models, Animal; Furans - pharmacology; Furans - therapeutic use; Heme Oxygenase-1 - antagonists & inhibitors; Heme Oxygenase-1 - metabolism; Immunology; Internal Medicine; Lignans - pharmacology; Lignans - therapeutic use; Lipopolysaccharides - toxicity; Male; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - physiology; Membrane Proteins - antagonists & inhibitors; Membrane Proteins - metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide Synthase Type II - antagonists & inhibitors; Nitric Oxide Synthase Type II - metabolism; Oxidative Stress - drug effects; Oxidative Stress - physiology; Pathology; Pharmacology/Toxicology; Protective Agents - pharmacology; Protective Agents - therapeutic use; Rheumatology
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-015-0115-3

Arctigenin, a bioactive component of Arctium lappa (Nubang), has anti-inflammatory activity. Here, we investigated the effects of arctigenin on lipopolysaccharide (LPS)-induced acute lung injury. Mice were divided into four groups: control, LPS, LPS + DMSO, and LPS + Arctigenin. Mice in the LPS + Arctigenin group were injected intraperitoneally with 50 mg/kg of arctigenin 1 h before an intratracheal administration of LPS (5 mg/kg). Lung tissues and bronchoalveolar lavage fluids (BALFs) were collected. Histological changes of the lung were analyzed by hematoxylin and eosin staining. Arctigenin decreased LPS-induced acute lung inflammation, infiltration of inflammatory cells into BALF, and production of pro-inflammatory cytokines. Moreover, arctigenin pretreatment reduced the malondialdehyde level and increased superoxide dismutase and catalase activities and glutathione peroxidase/glutathione disulfide ratio in the lung. Mechanically, arctigenin significantly reduced the production of nitric oxygen and inducible nitric oxygen synthase (iNOS) expression, enhanced the expression of heme oxygenase-1, and decreased the phosphorylation of mitogen-activated protein kinases (MAPKs). Arctigenin has anti-inflammatory and antioxidative effects on LPS-induced acute lung injury, which are associated with modulation of MAPK, HO-1, and iNOS signaling.