中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (5): 865-869.doi: 10.3969/j.issn.1673-8225.2011.05.025

• 移植与中医药 transplantation and traditional Chinese medicine • 上一篇    下一篇

落新妇甙对肝缺血再灌注损伤的保护作用

慕  宁,江  艺,张绍庚,陈少华,吕立志,张  坤,杨  芳,张小进,蔡秋程,潘  凡   

  1. 解放军南京军区福州总院肝胆外科,福建省福州市   350025
  • 收稿日期:2010-07-23 修回日期:2010-09-10 出版日期:2011-01-29 发布日期:2011-01-29
  • 通讯作者: 江艺,博士,主任医师,解放军南京军区福州总院肝胆外科,福建省福州市 350025 jiangyi183@ yahoo.com.cn
  • 作者简介:慕宁☆,男,1976年,甘肃省兰州市人,汉族,2008年解放军第二军医大学毕业,博士,主治医师,主要从事肝胆外科及肝移植临床及基础研究。 mnwsq@163. com

Protective effect of astilbin on liver ischemia-reperfusion injury

Mu Ning, Jiang Yi, Zhang Shao-geng, Chen Shao-hua, Lü Li-zhi, Zhang Kun, Yang Fang, Zhang Xiao-jin, Cai Qiu-cheng, Pan Fan   

  1. Department of Hepatobiliary Surgery, Fuzhou General Hospital of Nanjing Military Command of Chinese PLA, Fuzhou  350025, Fujian Province, China
  • Received:2010-07-23 Revised:2010-09-10 Online:2011-01-29 Published:2011-01-29
  • Contact: Jiang Yi, Doctor, Chief physician, Department of Hepatobiliary Surgery, Fuzhou General Hospital of Nanjing Military Command of Chinese PLA, Fuzhou 350025, Fujian Province, China jiangyi183@yahoo. com.cn
  • About author:Mu Ning☆, Doctor, Attending physician, Department of Hepatobiliary Surgery, Fuzhou General Hospital of Nanjing Military Command of Chinese PLA, Fuzhou 350025, Fujian Province, China mnwsq@163.com

摘要:

背景:肝脏是对缺血再灌注损伤最敏感的器官之一。黄酮类化合物落新妇甙可作为递氢体清除氧自由基,从而可能在减轻肝脏缺血再灌注损伤等方面发挥作用。
目的:观察落新妇甙对肝脏热缺血再灌注损伤的保护作用,对其机制进行初步探讨。
方法:C57BL/6小鼠随机分为4组:假手术组、模型组、小剂量干预组和大剂量干预组。干预组小鼠于缺血前24 h和1 h分别给予10或40 mg/kg的落新妇甙腹腔注射,然后建立70%部分肝缺血再灌注模型。采集血液和肝脏组织样本。检测血清丙氨酸氨基转移酶活性,ELISA测血清肿瘤坏死因子α水平,化学比色法测定肝组织中超氧化物歧化酶、丙二醛含量。肝脏组织病理学检测。Westernblot检测肝组织中肿瘤坏死因子α蛋白含量,RT-PCR检测肿瘤坏死因子α mRNA。
结果与结论:落新妇甙干预能有效降低血清丙氨酸氨基转移酶水平,干预组肝组织丙二醛含量较模型对照组明显下降(P < 0.01);而超氧化物歧化酶含量明显上升(P < 0.01);干预组血清肿瘤坏死因子α含量较模型组对照组明显下降(P < 0.01);小、大剂量干预组肝组织中肿瘤坏死因子α蛋白表达与模型组模型对照组比较渐次降低,与半定量RT-PCR结果相符(小剂量干预组P < 0.05,大剂量干预组P < 0.01)。落新妇甙保护肝脏热缺血再灌注损伤显示出剂量-效应关系趋势。结果提示,落新妇甙干预能减轻小鼠肝脏热缺血再灌注损伤后的炎症反应和脂质过氧化损伤,有效改善肝功能和肝脏病理损害;机制可能在于其能抑制缺血再灌注损伤肝组织中肿瘤坏死因子α的高表达。

关键词: 落新妇甙, 肝脏, 缺血再灌注损伤, 丙氨酸氨基转移酶, 丙二醛, 超氧化物歧化酶, 肿瘤坏死因子&alpha

Abstract:

BACKGROUND: Liver is one of the most sensitive organs to ischemia-reperfusion injury. Astilbin is one of the three flavanonols isolated from the ethanol extract of rhizome, which have strong function of antioxidant and can be used as delivery of hydrogen to scavenging oxygen free radicals, resulting in anti-inflammatory and reducing ischemia-reperfusion injury.
OBJECTIVE: To investigate the protective effect and mechanism of astilbin on liver warm ischemia-reperfusion injury.
METHODS: C57BL/6 mice were randomly divided into four groups: sham-operated, model control, low dosage astilbin group (10 mg/kg) and large dosage astilbin (40 mg/kg) group. At 24 hours and 1 hour before ischemia, treatment group mice were intraperitoneally injected 10 or 40 mg/kg astilbin. Then the hepatic ischemia-reperfusion models of 70 percent of liver were established. The partial hepatic lobe, blood and liver tissue samples were collected from the experimental groups. Serum alanine aminotransferase (ALT) activity was detected by ELISA. The content of malonaldehyde (MDA) and superoxide dismutase (SOD) in liver tissues were detected by chemo-chromatometry. The content of tumor necrosis factor α (TNF-α) in liver tissues were detected by western blot. TNF-α mRNA expression was detected by semiquantitative RT-PCR.
RESULTS AND CONCLUSION: Compared with the model group, serum ALT in both astilbin treatment groups was significantly decreased (P < 0.01). The content of MDA in liver tissues was significantly decreased in both treatment groups when compared with the model group (P < 0.01). And SOD levels significantly increased in treatment groups (P < 0.01). Serum TNF-α in both astilbin treatment groups were significantly decreased (P < 0.01). The protein content of TNF-α in liver tissues were gradually decreased in both treatment groups when compared with the model group, also lower in the large dosage group than in the low dosage group. Same trends were observed in the mRNA expression of these proteins showed by semiquantitative RT-PCR (low dosage group P < 0.05; large dosage group P < 0.01). The protective effect of astilbin on liver ischemia-reperfusion injury showed dose-response relationship. Treatment with astilbin can effectively reduce inflammatory response and the damage of lipid peroxidation induced by liver ischemia-reperfusion injury, and improves the mouse liver function and liver pathology damage. Depressing TNF-α expression in the liver tissue may be its mechanism.

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