Abstract
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.
Highlights
Intestinal ischemia reperfusion (I/R) is common in critically ill patients, which can result in intestinal injury, and injury in distant organs
We investigate the influence of ginsenoside Rb1 on lung injury and nuclear factor kappa B (NF-kB) activation induced by intestinal I/R
The edema, bleeding and villi irregularities could be found in the intestinal mucosa and submucosa in the I/R group
Summary
Intestinal ischemia reperfusion (I/R) is common in critically ill patients, which can result in intestinal injury, and injury in distant organs. Leukocyte-endothelial interaction plays a critical role in lung injury, recruiting and activating neutrophils to release inflammatory mediators. In this context, ICAM-1 exerts pivotal control over the movement of neutrophils into the injured site [2]. Ginsenoside Rb1, one of the panaxadiols, showed anti-stress effects in acute, chronic, and repeated stress models [8]. It has beneficial effects on cerebral [9], myocardial [10] ischemia reperfusion injury and intestinal I/R induced renal injury [11]. We investigate the influence of ginsenoside Rb1 on lung injury and NF-kB activation induced by intestinal I/R
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