Abstract
Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS). The aim of this study is to determine the effects of ginsenoside Rb1 on liver injury induced by intestinal I/R in rats. 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). Liver and intestinal histology was observed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) level in serum and malondialdehyde (MDA) level in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-alpha, MDA level and immunohistochemical expression of NF-kgr;B and intracellular adhesion molecule-1 (ICAM-1) in liver tissues was assayed. In addition, a western blot analysis of liver NF-kappaB expression was performed. Results indicated intestinal I/R induced intestinal and liver injury, which was characterized by increase of AST and ALT in serum, MDA level in intestine, MPO, TNF-alpha and MDA level and ICAM-1 and NF-kappaB expression in the liver tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated liver injury, decreased MPO, TNF-alpha and MDA level, NF-kappaB and ICAM-1 expression in liver tissues. In conclusion, ginsenoside Rb1 ablated liver injury induced by intestinal I/R by inhibiting NF-kappaB activation.
Highlights
Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS) (Antonsson et al, 1991; Poggetti et al, 1992a; Turnage et al, 1996; Pierro et al, 2004)
ginsenoside Rb1 (Rb1) inhibited the NF-κB activation in a dosedependent manner. These findings suggested the importance of NF-κB pathway in protective effects of Rb1 on liver injury induced by intestinal I/R
Many studies have demonstrated that inflammatory mediators are regulated by NF-κB, which is a key regulator of inflammatory gene expression in liver injury
Summary
Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS) (Antonsson et al, 1991; Poggetti et al, 1992a; Turnage et al, 1996; Pierro et al, 2004). Ischemia by itself induces little damage, reperfusion of the previously ischemic organ can yield to remote organ injury and life threatening multiple organ failure (Poggetti et al, 1992b; Amersi et al, 1999). The pathogenesis of multiple organ failure after intestinal I/R is multifactorial, but the development of oxidative injury with a subsequent systemic inflammatory response appears to play a pivotal role (Cuzzocrea et al, 2000; Kalia et al, 2001). It has been shown that NF-κB plays an important role in intestinal I/R (Yao et al, 2007)
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