Methanol extract of Antrodia camphorata protects against lipopolysaccharide-induced acute lung injury by suppressing NF-κB and MAPK pathways in mice.
Antrodia camphorata (AC) has been used as a herbal medicine for drug intoxication for the treatment of inflammation syndromes and liver-related diseases in Taiwan. This study demonstrates the protective effect of the methanol extract of AC (MAC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Mice were treated with MAC 1 h before the intratracheal (I.T.) instillation of LPS challenge model. Lung injury was evaluated 6 h after LPS induction. Pretreatment with MAC markedly improved LPS-induced histological alterations and edema in lung tissues. Moreover, MAC also inhibited the release of pro-inflammatory mediators such as nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6 at 6 h in the bronchoalveolar lavage fluid (BALF) during LPS-induced lung injury. Furthermore, MAC reduced total cell number and protein concentrations in the BALF the pulmonary wet/dry weight (W/D) ratio, and myeloperoxidase activity and enhanced superoxide dismutase (SOD) activity in lung tissues. MAC also efficiently blocked protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and phosphorylation of mitogen-activated protein kinases (MAPKs) and inhibited the degradation of nuclear factor-kappa B (NF-κB) and IκBα. This is the first investigation in which MAC inhibited acute lung edema effectively, which may provide a potential target for treating ALI. MAC may utilize the NF-κB and MAPKs pathways and the regulation of SOD activity to attenuate LPS-induced nonspecific pulmonary inflammation.
Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, College of Pharmacy, China Medical University , Taichung 404, Taiwan.
Guan-Jhong
GJ
Huang
Jeng-Shyan
JS
Deng
Chin-Chu
CC
Chen
Ching-Jang
CJ
Huang
Ping-Jyun
PJ
Sung
Shyh-Shyun
SS
Huang
Yueh-Hsiung
YH
Kuo
D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D000818:Animals; D055491:Antrodia / Q000737:chemistry*; D005260:Female; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides / Q000009:adverse effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000276:immunology; D016328:NF-kappa B / Q000235:genetics* / Q000276:immunology; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000276:immunology; D010936:Plant Extracts / Q000008:administration & dosage* / Q000302:isolation & purification; D020011:Protective Agents / Q000008:administration & dosage* / Q000302:isolation & purification; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010936:Plant Extracts; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; D020928:Mitogen-Activated Protein Kinases