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|標題:||Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-kappa B and STAT-1 activation||作者:||Hou, Y.C.
|關鍵字:||Silymarin;Cerebral ischemia-reperfusional (CI/R) injury;Cytokine;Signal transducer and activator of transcription-1 (STAT-1);Inducible;nitric oxide synthase (iNOS);Nuclear factor-kappa B (NF-kappa B);adhesion molecule-1;signal transducers;stroke;contributes;inhibition;mice;modulation;mechanisms;expression;management||Project:||Phytomedicine||期刊/報告no：:||Phytomedicine, Volume 17, Issue 12, Page(s) 963-973.||摘要:||
Silymarin and silibinin are bioactive components isolated from Silybum marianum. They have been reported to exhibit anti-oxidative and anti-inflammatory effects. Many studies revealed that drugs with potent anti-inflammatory potential can protect animals against inflammation-associated neurodegenerative disease, e.g., stroke. In this current work we established an animal model of acute ischemic stroke injury by inducing cerebral ischemic/reperfusion (CUR) in rats to elucidate whether silymarin or silibinin can protect animals from CUR injury. Pretreatment with silymarin, but not silibinin, dose-dependently (1-10 mu g/kg, i.v.) reduced CUR-induced brain infarction by 16-40% and improved neurological deficits in rats with a stroke. Elevated pathophysiological biomarkers for CUR-induced brain injury, including lipid peroxidation, protein nitrosylation, and oxidative stress, were all reduced by silymarin. In addition, expression of inflammation-associated proteins (e.g., inducible nitric oxide synthase, cyclooxygenase-2 and myeloperoxidase), and transcriptional factors (e.g., nuclear factor (NF)-kappa B and signal transducer and activator of transcription (STAT)-1), as well as production of proinflammatory cytokine (e.g., interleukin-1 beta and tumor necrosis factor-alpha) was all significantly prevented by silymarin. Furthermore, an in vitro study on microglial BV2 cells showed that silymarin could inhibit nitric oxide and superoxide anion production, possibly by interfering with NF-kappa B nuclear translocation/activation. Likewise, silymarin pretreatment also inhibited I kappa B-alpha degradation and NF-kappa B nuclear translocation in brain tissues of ischemic rats. Our results reveal that silymarin, but not its active component silibinin, protected rats against CUR-induced stroke injury by amelioration of the oxidative and nitrosative stresses and inflammation-mediated tissue injury through impeding the activation of proinflammatory transcription factors (e.g., NF-kappa B and STAT-1) in the upregulation of proinflammatory proteins and cytokines in stroke-damaged sites. In conclusion, silymarin displays beneficial effects of preventing inflammation-related neurodegenerative disease, e.g., stroke, which needs further investigation and clinical evidences. (C) 2010 Elsevier GmbH. All rights reserved.
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