Protective effect of ginsenoside Rb1 against lung injury induced by intestinal ischemia-reperfusion in rats.
Intestinal ischemia-reperfusion (I/R) is a critical event in the pathogenesis of multiple organ dysfunction syndromes (MODS). The lungs are some of the most vulnerable organs that are impacted by intestinal I/R. The aim of this study is to investigate whether ginsenoside Rb1 can ameliorate remote lung injury induced by intestinal I/R. Adult male Wistar rats were randomly divided into four groups: (1) a control,  sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Intestinal and lung histology was observed. The malondialdehyde (MDA) levels in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA levels, wet/dry weight ratio and immunohistochemical expression of intracellular adhesion molecule-1 (ICAM-1) in lung tissues were assayed. In addition, a western blot of lung NF-kB was performed. Results indicated that intestinal I/R induced intestinal and lung injury, which was characterized by increase of MDA levels and pathological scores in intestinal tissues and MPO, TNF-α , MDA levels, wet/dry weight ratio and ICAM-1, NF-kB expression in the lung tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated intestinal and lung injury, decreased MPO, TNF-α, MDA levels, wet/dry weight ratio, ICAM-1 and NF-kB expression in lung tissues. In conclusion,  ginsenoside Rb1 ameliorated the lung injuries by decreasing the NF-kB activation-induced inflammatory response.
Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, Hubei, China.
Jin
J
Wang
Lifen
L
Qiao
Shusheng
S
Li
Guangtian
G
Yang
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D000975:Antioxidants / Q000008:administration & dosage*; D036145:Ginsenosides / Q000008:administration & dosage*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D055370:Lung Injury / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008638:Mesenteric Arteries / Q000473:pathology; D008641:Mesenteric Vascular Occlusion / Q000150:complications / Q000188:drug therapy; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy*; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D036145:Ginsenosides; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; C442759:ginsenoside Rb1; D009195:Peroxidase