Green tea modulates reserpine toxicity in animal models
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概要
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Reserpine, a natural product extracted from Rauwolfia serpintina or Rauwolfia vomitoria, is a known dopamine depleter that inhibits several neurotransmitters. Reserpine has been used clinically to control hypertension, schizophrenia, insomnia and insanity. The use of this drug, however, has been limited because of its side effects which include oxidative damage to organs, including the liver. Green tea catechins are potent antioxidants that have the potential to counteract reserpine induced oxidative stress. This study investigated the merits of administering green tea concurrently with reserpine to prevent oxidative hepatic damage in Sprague-Dawely (SD) rats. Reserpine was found to cause hepatic damage, with elevated levels of oxidative stress markers, such as Thiobarbituric Acid Reactive Substances (TBARS), transaminases and cholesterol. Reserpine also induced hepatic ultra-structural damage in the cytoplasmic membrane, nuclear envelope, endoplasmic reticulum (rER), ribosomal stripping and mitochondria. Electron microscopy examination showed revival of liver cells as a result of green tea extract administration to experimental rats.
- 2009-02-01
著者
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Al-Bloushi Shaima
Department of Biological Sciences, Faculty of Science, Kuwait University
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Safer Abdel-Majeed
Department of Biological Sciences, Faculty of Science, Kuwait University
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Afzal Mohammed
Department of Biological Sciences, Faculty of Science, Kuwait University
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Mousa Shaker
The Pharmaceutical Research Institute at Albany College of Pharmacy
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Safer Abdel-majeed
Department Of Biological Sciences Faculty Of Science Kuwait University
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Afzal Mohammed
Department Of Biological Sciences Faculty Of Science Kuwait University
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Al-bloushi Shaima
Department Of Biological Sciences Faculty Of Science Kuwait University
関連論文
- Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells
- Green tea modulates reserpine toxicity in animal models