Ginsenoside Rg1 protects mouse liver against ischemia-reperfusion injury through anti-inflammatory and anti-apoptosis properties
Ginsenoside Rg1 protects mouse liver against ischemia-reperfusion injury through anti-inflammatory and anti-apoptosis properties
复制标题
人参皂苷 Rg1 通过抗炎和抗凋亡特性保护小鼠肝脏免受缺血再灌注损伤。
DOI：
10.1016/j.jss.2014.03.067
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发表时间：
2014-09-01
影响因子：
2.2
通讯作者：
Deng, Xiaoming
中科院分区：
文献类型：
--
作者：
Tao, Tianzhu;Chen, Feng;Deng, Xiaoming
背景：人参皂苷Rg 1是人参的主要有效成分，具有多种药理活性。本研究旨在探讨人参皂甙Rg 1对肝脏缺血再灌注（IR）损伤的影响及其可能的机制。材料和方法：采用门静脉阻断和肝动脉阻断1h，再灌注6 h的方法建立肝脏热IR损伤模型。将18只小鼠随机分为假手术组、IR组和IR + Rg 1组（每组6只）。小鼠在缺血损伤前接受静脉内剂量为20 mg/kg的Rg 1或等体积的生理盐水。收集肝脏样品和血清用于分析。测定血清转氨酶、组织病理学和细胞凋亡。通过实时定量逆转录聚合酶链反应（qRT-PCR）测量细胞因子。Western blotting检测核因子-κ B（NF-κ B）p65的磷酸化水平。此外，还研究了Rg 1在体外模拟IR模型中的作用。Rg 1（100 μ g/mL和500 μ g/mL）在缺氧前1h给药，再灌注12 h后检测细胞凋亡率。结果：肝脏IR损伤导致肝脏氨基转移酶活性显著升高，肝细胞凋亡和坏死，促炎细胞因子产生。Rg 1预处理保护小鼠免受IR诱导的肝损伤。高剂量Rg 1（500 μ g/mL）处理组与低剂量组和对照组相比，细胞凋亡明显减少（P均< 0.001）。IR组NF-κ B p65的磷酸化水平显著升高，Rg 1干预可抑制NF-κ B p65的磷酸化水平。结论：Rg 1预处理可减少肝细胞凋亡，抑制炎症反应，其机制可能与NF-κ B信号通路有关。Rg 1可能为治疗IR诱导的肝损伤提供一种新的治疗策略。(C)2014爱思唯尔公司All rights reserved.
Background: Ginsenoside Rg1, the major effective component of ginseng, possesses a variety of pharmacologic activities. The objective of this study was to investigate the effects of Rg1 on liver ischemia-reperfusion (IR) injury and explore its potential mechanisms.Materials and methods: Liver warm IR injury was achieved by occluding the portal vein and hepatic artery for 1 h followed by 6-h reperfusion. Eighteen mice were equally randomized into three groups: sham group, IR group, and IR plus Rg1 group (n = 6 mice per group). Mice received an intravenous dose of 20 mg/kg Rg1 or an equivalent volume of saline before ischemic insult. Liver samples and serum were collected for analyses. Serum aminotransferase, histopathology, and apoptosis were determined. Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylation of nuclear factor kappa B (NF-kappa B) p65 was assessed by Western blotting. In addition, the effect of Rg1 in a simulated IR model in vitro was also investigated. Rg1 (100 ug/mL and 500 ug/mL) was administered 1 h before hypoxia insult, and then apoptosis was measured after 12-h reperfusion.Results: Liver IR injury led to a dramatic increase in aminopherase activity, apoptosis and necrosis of hepatocytes, and production of proinflammatory cytokines. Pretreatment with Rg1 protected mice from IR-induced liver injury. Treatment with a high-dose Rg1 (500ug/mL) significantly suppressed apoptosis compared with a lower dose or control (both P < 0.001). Phosphorylation of NF-kappa B p65 was increased significantly in IR group, and administration with Rg1 suppressed the level of phosphorylation.Conclusions: Pretreatment of mice with Rg1 reduced hepatocellular apoptosis and inhibited inflammatory response, which was in part through the NF-kappa B signaling pathway. Rg1 may provide a novel therapeutic strategy for the treatment of IR-induced liver injury. (C) 2014 Elsevier Inc. All rights reserved.