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首页> 外文期刊>Inflammation >Anti-inflammation Effects of Cordyceps sinensis Mycelium in Focal Cerebral Ischemic Injury Rats
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Anti-inflammation Effects of Cordyceps sinensis Mycelium in Focal Cerebral Ischemic Injury Rats

机译:冬虫夏草菌丝体对局灶性脑缺血大鼠的抗炎作用

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摘要

Brain ischemia–reperfusion (IR) triggers a complex series of biochemical events including inflammation. To test the neuroprotective efficacy of Cordyceps sinensis mycelium (CSM) in a rat model of focal cerebral IR, ischemic animals were treated with CSM. They were evaluated at 24 h after reperfusion for neurological deficit score. Furthermore, the mechanism of the anti-inflammatory potential of CSM in the regulation of nuclear factor kappaB, polymorphonuclear cells (PMN), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), adhesion molecule (ICAM-1), and cyclooxygenase-2 (COX-2) was determined by ELISA and immunohistochemistry. CSM significantly inhibited IR-induced up-regulation of NF-kappaB activation and the brain production of IL-1β, TNF-α, iNOS, ICAM-1, and COX-2. Moreover, CSM suppressed infiltration of PMN. The study demonstrates the neuroprotective potential of CSM inhibition through anti-inflammation in a rat model of ischemia–reperfusion.
机译:脑缺血再灌注(IR)引发一系列复杂的生化事件,包括炎症。为了测试冬虫夏草菌丝体(CSM)在局灶性脑IR模型中的神经保护作用,用CSM治疗缺血动物。在再灌注后24小时评估他们的神经功能缺损评分。此外,CSM的抗炎潜能在调节核因子κB,多形核细胞(PMN),白介素-1β(IL-1β),诱导型一氧化氮合酶(iNOS),肿瘤坏死因子-α(TNF)的机制中-α),粘附分子(ICAM-1)和环氧合酶2(COX-2)通过ELISA和免疫组织化学测定。 CSM显着抑制IR诱导的NF-κB激活和脑中IL-1β,TNF-α,iNOS,ICAM-1和COX-2的上调。此外,CSM抑制了PMN的渗透。该研究证明了在缺血再灌注大鼠模型中通过抗炎作用抑制CSM的神经保护作用。

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