法舒地尔对大鼠脑缺血再灌注损伤炎症反应的影响

被引:19
作者
吴建华
方云祥
机构
[1] 中南大学药学院药理学教研室
关键词
法舒地尔; 脑缺血; NF-κB; 炎症;
D O I
暂无
中图分类号
R96 [药理学];
学科分类号
100602 ; 100706 ;
摘要
目的:观察法舒地尔对大鼠脑缺血再灌注损伤炎症反应的影响,探讨其抗炎机制。方法:大脑中动脉线栓法(MCAO)制作大鼠局灶性脑缺血再灌注损伤模型,缺血1.5h再灌注24h。法舒地尔术前腹腔注射给药15mg/kg,术后12h再次给药。术后对大鼠神经功能进行评分,TTC染色观察脑梗死体积;用干湿重法测定脑含水量;分光光度法测定髓过氧化物酶(MPO)活性;伊文思兰法(EB)测定血脑屏障的损伤程度;免疫组化检测大鼠脑缺血区细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、NF-κB p65的表达;ELISA法检测IL-8的含量;Western blot法检测单核细胞趋化蛋白-1(MCP-1)和核抽提物中NF-κBp65蛋白的表达;RT-PCR检测NF-κB p65mRNA的表达。结果:法舒地尔能明显改善脑缺血再灌注损伤大鼠神经缺陷症状,缩小脑梗死体积,明显降低缺血侧脑组织的含水量、EB含量及MPO活性;显著抑制ICAM-1、VCAM-1、IL-8和MCP-1蛋白的表达;降低NF-κB p65mRNA和蛋白的表达;减少脑组织核抽提物中NF-κB p65的蛋白量(P<0.05vsMCAO组)。结论:法舒地尔通过抑制NF-κBp65的活化,进而抑制黏附分子及趋化因子的表达,减轻脑缺血再灌注损伤的炎症反应。
引用
收藏
页码:377 / 383
页数:7
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