摘要
目的:评价大黄素抗脑缺血损伤作用,并从细胞因子水平及表达方面探讨其抑制炎性级联反应机制。方法:将大鼠分为假手术组、模型组、川芎嗪组、大黄素组(低、中、高剂量)。线栓法制备局灶性脑缺血6 h模型。观察神经症状积分、脑组织含水量、梗死面积变化,放射免疫法测定脑组织TNF-α,IL-1β,TGF-β水平,免疫组织化学法测定TNF,VCAM-1表达,原位杂交法测定VCAM-1-mRNA表达。结果:与假手术组比较,模型组大鼠神经症状积分和脑含水量及梗死面积增加,脑组织TNF-α和IL-1β水平增高、TGF-β水平降低,TNF和VCAM-1的表达增强(P<0.01);大黄素各组神经症状积分和脑含水量及梗死面积明显降低,以低剂量组尤为显著;大黄素低剂量组和川芎嗪组TNF-α和IL-1β水平及TNF,ICAM-1表达明显降低(P<0.01),TGF-β水平增高(P<0.01),大黄素低剂量组较川芎嗪组尤为显著。结论:由多种细胞因子介导的炎性级联反应增强和TGF的保护作用减弱是脑缺血损伤的重要机制。大黄素抗脑缺血损伤作用机制可能是通过抑制脑组织炎性级联反应和提高脑保护因子如TGF水平而实现的。
Objective： To assess emodin antagonism to cerebral ischemia injury, and to discuss the mechanism of errlodin inhibiting the inflammatory cascade reaction from the levels and expressions of cytokines,Method： Rats were divided into sham-operated group, model group, Ligustrazine group and emodin groups （ low, middle, high dosage）. After focal cerebral ischemic model of cerebral middle artery occlusion was duplicated with nylon thread, we took the speciments after ischemia 6 hours, observed the changes of the evaluating score of neural symptoms, brain water ratio and cerebral infarction area, determined the levels of TNF-α, IL-β and TGF-β in rats brain tissue by radioimmunoassay, detected the expressions of TNF-α and VCAM-1 by immunohistochemistry, and measured VCAM-1-mRNA expression by in-situ hybridization. Result： Compared with sham-operated group, the evaluating score of neural symptoms, brain water ratio and cerebral infarction area of rats in model group were higher（ P 〈0.01 ）, the levels of TNF-α and IL-β of rats brain tissue in model group increased, while the lev- el of TGF-β was lower, and the expressions of TNF-α and VCAM-1 increased P 〈 0.01 ）. The evaluating score of neural symptoms, brain water ratio and cerebral infarction area improved obviously in every emodin group, especially in emodin low dosage group. Levels of TNF-α, IL-β and the expressions of TNF-α and ICAM-1 in emodin low dosage group and Ligustrazine group were lower, while the level of TGF-β was higher. Compared with Ligustrazine group, the changes aboved are more significant in emodin low dosage group（P 〈 0.01）. Conclusion： The increase of inflammatory cascade reaction mediated by various cytokines such as TNF, IL-β, ICAM-1 and the decrease of TGF protection are the important mechanism of cerebral ischemia injury. The mechanism of emodin antagonism to cerebral ischemia injury may be implemented by inhibiting inflammatory cascade reaction and increasing the brain protective factors, such as TGF.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2005年第24期1939-1943,共5页
China Journal of Chinese Materia Medica
基金
河南省杰出人才创新基金项目(0221001700)
高校创新人才基金项目(2000-10)
关键词
脑缺血
大鼠
大黄素
炎性级联反应
cerebral ischemia
frats
emodin
inflammatory cascade reaction
