School of Basic Medical Sciences, Beijing University of Chinese Medicine, Beijing, 100102, China.
Inflammation. 2011 Dec;34(6):639-44. doi: 10.1007/s10753-010-9273-5.
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.
脑缺血再灌注(IR)引发了一系列复杂的生化事件,包括炎症。为了在局灶性脑 IR 大鼠模型中测试冬虫夏草菌丝体(CSM)的神经保护功效,对缺血动物进行了 CSM 治疗。在再灌注后 24 小时对它们进行神经功能缺损评分评估。此外,通过 ELISA 和免疫组织化学测定,确定了 CSM 在调节核因子 kappaB、多形核细胞(PMN)、白细胞介素-1β(IL-1β)、诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)、细胞间黏附分子(ICAM-1)和环氧化酶-2(COX-2)方面的抗炎潜力的机制。CSM 显著抑制了 IR 诱导的 NF-kappaB 激活和大脑中 IL-1β、TNF-α、iNOS、ICAM-1 和 COX-2 的产生。此外,CSM 抑制了 PMN 的浸润。该研究表明 CSM 通过抑制炎症在缺血再灌注大鼠模型中具有神经保护潜力。