Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats

Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats
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DOI:
10.1016/j.freeradbiomed.2004.04.022
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发表时间:
2004-08-01
影响因子:
7.4
通讯作者:
Oztas, E
Oztas, E
中科院分区:
医学1区
文献类型:
--
作者:
Ilhan, A;Akyol, O;Oztas, E

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由于已知氧化损伤参与炎症和自身免疫介导的组织破坏,因此调节氧自由基的产生代表了治疗炎症和自身免疫性疾病的新途径。中枢神经系统组织特别容易受到氧化损伤,提示氧化在多发性硬化症(MS)及其动物模型实验性自身免疫性脑脊髓炎(EAE)的发病机制中起重要作用。咖啡酸苯乙酯(CAPE)是蜜蜂蜂胶的一种有效成分,具有抗氧化、抗炎、抗病毒和抗癌活性。我们之前报道过CAPE抑制兔脊髓组织缺血再灌注损伤和氧化应激。因此,本研究考察了CAPE对EAE大鼠氧化组织损伤的影响。CAPE治疗可显著抑制EAE诱导的活性氧(ROS)产生,改善大鼠临床症状。上述结果提示,CAPE的抗炎作用可能是通过抑制核因子κ b的激活,在转录水平上抑制ROS的产生,并直接抑制诱导型一氧化氮合酶的催化活性。(C) 2004爱思唯尔公司版权所有。
Because oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase. (C) 2004 Elsevier Inc. All rights reserved.