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大黄素甲醚对大鼠脑缺血再灌注损伤的拮抗作用 被引量:12

Protective effects of physcion against cerebral injury induced by ischemiareperfusion in rats
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摘要 目的:探讨大黄素甲醚对脑缺血再灌注后IL-1β含量和ICAM-1及caspase-3表达的影响。方法:91只SD大鼠随机分为正常组(normal),假手术组(sham),模型组(model),大黄素甲醚大剂量(PHD)及小剂量(PLD)组。采用线栓法复制大鼠右侧大脑中动脉脑缺血再灌注模型,用放射免疫法测定病变侧脑组织IL-1β的含量,用免疫组织化学方法测定ICAM-1和caspase-3表达的变化,并进行组织病理学观察。结果:Model组再灌注6h病变侧IL-1β含量明显升高且达高峰,再灌注24h病变侧ICAM-1、caspase-3表达明显升高,中性粒细胞附壁浸润明显;大黄素甲醚PHD组再灌注12h、24h病变侧IL-1β、ICAM-1和caspase-3表达明显低于model组相应时段(P<0.05或P<0.01),中性粒细胞附壁浸润较少。结论:大黄素甲醚可降低脑缺血再灌注后IL-1β、ICAM-1和caspase-3水平,减轻脑缺血再灌注损伤。 AIM: To explore the effect of physcion (P) on the level of 1L - 1 β and expression of ICAM - 1 and easpase - 3 duting cerebral ischemia - repeffusion injury. METHODS: The 91 healthy adult SD rats were selected, and were randomly divided into normal group, sham- operated group, cerebral ischemia- repeffusion group (model), low- dose physcion (PLD) and high- dose physcion (PHD) treatment group. The level of IL- 1β was detected by radioimmunoassay. The expression of ICAM - 1 and caspase- 3 was detected by immunohistochemistry. The changes of tissue pathology were also investigated. RESULTS: The level of 1L - 1β reached the peak at 6 h after ischemia - reperfusion ( IR). The protein expression of ICAM - 1 and caspase - 3 reached the peak at 24 h after 1R. The level of IL- 1β and the protein expression of 1CAM- 1 and caspase- 3 in PHD group decreased obviously compared with those in model group ( P 〈 0.05 or P 〈 0.01 ), infiltration and adhesiveness of neutrophils were less serious at the same time. CONCLUSION: Physcion decreases the level of IL- 1β and the protein expression of ICAM - 1 and caspase - 3 to protect brain tissue from cerebral ischemia- reperfusion injury.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2005年第9期1829-1833,共5页 Chinese Journal of Pathophysiology
关键词 大黄素甲醚 脑缺咀 再灌注损伤 白细胞介素1 胞间粘附分子1 半胱氨酸天冬氨酸蛋白酶3 Physcion Brain ischemia Repeffusion injury Interleukin-1 Intercellular adhesion molecule-1 Caspase3
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参考文献13

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二级参考文献43

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