Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (5): 865-869.doi: 10.3969/j.issn.1673-8225.2011.05.025

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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

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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