首页> 外文会议>Annual Rocky Mountain Bioengineering Symposium >THYMOQUINONE INHIBITS THE ACTIVATION OF NF-κB N THE BRAIN AND SPINAL CORD OF EXPERIMENTAL UTOIMMUNE ENCEPHALOMYELITIS
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THYMOQUINONE INHIBITS THE ACTIVATION OF NF-κB N THE BRAIN AND SPINAL CORD OF EXPERIMENTAL UTOIMMUNE ENCEPHALOMYELITIS

机译:胸腺量抑制了NF-κBn的脑和脊髓的激活实验性utoimmune脑脊髓炎

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The present study was done to investigate the possible effects of thymoquinone on the inhibition of activation of NF-KB in experimental autoimmune encephalomyelitis in the rat model of multiple sclerosis. Experimental autoimmune encephalomyelitis was induced in Lewis rats by injecting myelin basic protein emulsified in complete freund's adjuvant. Several parameters including clinical signs, peri vascular cuffing and infiltration of mononuclear cells in the brain and spinal cord, glutathione levels in the red blood cells and inhibition of the activation of NF-KB were determined to assess the degree of protection. The study showed that treatment of rats with thymoquinone 1mg/kg/day concomitant to myelin basic protein and after the appearance of clinical signs resulted in preventing and ameliorating experimental autoimmune encephalomyelitis. Thymoquinone was able to counter perivascular cuffing and infiltration of mononuclear cells in the brain and spinal cord, increase the red blood cell glutathione, and inhibit the activation of NF-KB in the brain and spinal cord. These results were consistent with the clinical signs and suggest a beneficial effect of thymoquinone against experimental autoimmune encephalomyelitis in the rat model of multiple sclerosis.
机译:本研究进行了探讨紫醌对多发性硬化大鼠大鼠模型中实验自身免疫脑髓炎中NF-KB活化的抑制的可能影响。通过在完全弗氏佐剂中注射髓鞘碱性蛋白质,在Lewis大鼠中诱导实验性自身免疫性脑膜炎。几个参数包括临床症状,脑血管刺激和单核细胞中单核细胞的渗透,确定红细胞中的谷胱甘肽水平和NF-KB活化的抑制,以评估保护程度。研究表明大鼠百里醌为1mg / kg /天的伴随该处理,髓磷脂碱性蛋白和临床症状出现后导致预防和改善实验性自身免疫性脑脊髓炎。胸腺量能够对脑和脊髓中单核细胞进行反击和浸润,增加红细胞谷胱甘肽,并抑制脑和脊髓中NF-KB的活化。这些结果与临床症状一致,表明紫喹诺酮对多发性硬化症大鼠模型中的实验性自身免疫性脑髓炎的有益作用。

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