Green tea extract ameliorates reperfusion injury to rat livers after warm ischemia in a dose-dependent manner
✍ Scribed by Rui Liang; Arash Nickkholgh; Michael Kern; Heinz Schneider; Steffen Benzing; Markus Zorn; Markus W. Büchler; Peter Schemmer
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 310 KB
- Volume
- 55
- Category
- Article
- ISSN
- 1613-4125
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✦ Synopsis
Abstract
Scope: Polyphenolic constituents of green tea (Camellia sinensis) have been shown to be potent scavengers of reactive oxygen species (ROS). Thus, this study was designed to assess its effects after liver ischemia–reperfusion.
Methods and results: Fasted Sprague–Dawley rats were gavaged with different concentrations of green tea extract (GTE) 2 h before 90 min of warm ischemia of the left lateral liver lobe (30% of liver). Controls were given the same volume of Ringer's solution. A preparation of pentobarbital sodium (intraperitoneal) and ketamine (intramuscular) was used for anesthesia. After reperfusion, transaminases, liver histology, hepatic microcirculation, and both phagocytosis of latex bead particles as well as the expression of tumor necrosis alpha (TNF‐α) to index cellular activation were investigated. Furthermore, the expression of superoxide dismutase (Mn‐SOD) was assessed. After 90 min of warm ischemia aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) increased dramatically to 1946±272/3244±757 U/L, 1680±134/2080±379 U/L, and 7857±1851/2036±1193 U/L at 2/6 h, respectively. GTE (200 mg/kgbody weight) significantly prevented this increase in a dose‐dependent manner by 21–51% at 2 h and 29–34% at 6 h, respectively. Histology confirmed the protective effects while both TNF‐α expression and phagocytosis of latex beads by Kupffer cells (KCs) were significantly reduced. GTE intake significantly increased the expression of manganese superoxide dismutase. In vivo microscopy revealed improved acinar and sinusoidal perfusion after GTE.
Conclusion: Preconditioning with a single oral dose of GTE ameliorates ischemia–reperfusion injury in liver. Decreased cellular activation and improved microcirculation are the proposed mechanisms.