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Silymarin neuroprotective effects.
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| Article Type: | Report |
| Subject: |
Cerebral ischemia
(Care and treatment) Cerebral ischemia (Research) Medicine, Botanic (Health aspects) Medicine, Herbal (Health aspects) Milk thistle (Usage) Milk thistle (Health aspects) Milk thistle (Chemical properties) Milk thistle (Research) |
| Author: | Finney-Brown, Tessa |
| Pub Date: | 12/22/2010 |
| Publication: | Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2010 National Herbalists Association of Australia ISSN: 1033-8330 |
| Issue: | Date: Winter, 2010 Source Volume: 22 Source Issue: 4 |
| Topic: | Event Code: 310 Science & research |
| Geographic: | Geographic Scope: Australia Geographic Code: 8AUST Australia |
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| Accession Number: | 254971797 |
| Full Text: |
Hou Y, Liou K, Chem C, Wang Y, Liao J, Chang S, Chou Y, Shen Y.
2010 Preventive effect of silymarin in cerebral ischemia
reperfusion-induced brain injury in rats possibly through impairing
NF-[kappa]B and STAT-1 activation. Phytomed 17:12;963-73. Silymarin and silybin are some of the major bioactive constituents of St Marys Thistle (Silybum marianum), displaying potent anti-inflammatory and antioxidative activity. These effects may be useful in reducing neurological injury induced by ischemic stroke. The major pathological mechanism underlying ischemic/ reperfusion injury to brain tissue is a phenomenon known as 'excitotoxicity' in which excessive release of glutamate (which builds up in the extracellular spaces after stroke onset) causes an inappropriate activation of ionotropic N-methyl-d-aspartate (NMDA) receptors in the brain. It basically excites neurons to death via excessive production of reactive oxygen species (ROS). A number of free radical producing enzyme systems are involved. ROS and reactive nitrogen species damage brain tissue via lipid peroxidation or protein nitrosulation of cell organelles and cell membrane, as well as by direct attacks on DNA. In this research investigators set out to determine whether pre or post treatment with the flavonoids silymarin and silybin could protect mice from cerebral ischemic/reperfusion (CI/R) injury. Solutions containing silymarin or silybin, along with a sham solution, were given intravenously 15 min before (pretreat) or 60 min after (posttreat) RMCA occlusion at three different doses (1, 5 or 10 mcg/kg). Silymarin but not silybin dose dependently (1-10 mcg/ kg iv) reduced CI/R induced brain infarction by 16-40%. It also reduced pathophysiological biomarkers of brain injury (normally elevated in CI/R), including lipid peroxidation, protein nitrosylation and oxidative stress. Silymarin, but again not silybin, prevented expression of inflammation associated proteins and transcriptional factors, as well as proinflammatory cytokine production. This flavonoid may inhibit nitric oxide and superoxide anion production by interfering with NF-[kappa]B nuclear translocation/activation. This is the first piece of research to show that silymarin may reduce ischemic tissue damage to the brain in addition to its already proven ability to protect the kidney, myocardium and liver from these types of injury. Silymarin had more protective effects when given prior to injury, potentially indicating that it may function via indirect modulation of early inflammatory signals rather than by direct interference with nitric oxide synthase. The promising results of the trial suggest that further investigation into the extract as a neuroprotective agent is warranted. Tessa Finney-Brown MNHAA tessafinneybrown@gmail.com |
| Gale Copyright: | Copyright 2010 Gale, Cengage Learning. All rights reserved. |
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