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Ginsenoside Rb1 attenuates intestinal ischemia-reperfusion-induced liver injury by inhibiting NF-κB activation

机译:人参皂苷Rb1通过抑制NF-κB活化来减轻肠缺血再灌注所致的肝损伤

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摘要

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-α, MDA level and immunohistochemical expression of NF-κB and intracellular adhesion molecale-1 (ICAM-1) in liver tissues was assayed. In addition, a western blot analysis of liver NF-κB 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-α and MDA level and ICAM-1 and NF-κB expression in the liver tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated liver injury, decreased MPO, TNF-α and MDA level, NF-κB and ICAM-1 expression in liver tissues. In conclusion, ginsenoside Rb1 ablated liver injury induced by intestinal I/R by inhibiting NF-κB activation.
机译:肠缺血再灌注(I / R)是多器官功能障碍综合征(MODS)发病机理中的重要事件。这项研究的目的是确定人参皂甙Rb1对大鼠肠I / R所致肝损伤的影响。将成年雄性Wistar大鼠随机分为四组:(1)对照组,假手术组(假手术组); (2)肠I / R组经历1小时的肠缺血和2小时的再灌注(I / R组); (3)再灌注前用20mg / kg人参皂苷Rb1治疗的组(Rb1-20组); (4)再灌注前用40 mg / kg人参皂甙Rb1治疗的组(Rb1-40组)。观察到肝和肠的组织学。测量血清中的天冬氨酸转氨酶(AST),丙氨酸转氨酶(ALT)和肠组织中的丙二醛(MDA)水平。检测肝组织中的髓过氧化物酶(MPO),TNF-α,MDA水平以及NF-κB和细胞内黏附分子1(ICAM-1)的免疫组织化学表达。另外,进行了肝NF-κB表达的蛋白质印迹分析。结果表明肠I / R引起肠和肝损伤,其特征是血清中AST和ALT升高,肠中MDA水平,MPO,TNF-α和MDA水平以及肝组织中ICAM-1和NF-κB表达增加。人参皂甙Rb1(20,40 mg / kg)改善了肝损伤,降低了肝组织中MPO,TNF-α和MDA的含量,NF-κB和ICAM-1的表达。总之,人参皂甙Rb1通过抑制NF-κB活化来减轻肠I / R诱导的肝损伤。

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