摘要
目的:建立大鼠缺氧缺血性脑损伤(HIBD)模型,将IκB通过腺病毒载体导入体内,探讨其对HIBD大鼠脑内NF-κB活性和TNF-α、IL-1表达的影响。方法:40只大鼠随机分为5组:I组(正常对照组),II组(HIBD损伤1d组),III组(HIBD损伤7d组),IV组(IκB干预1d组),V组(IκB干预7d组)。Western-blot检测脑细胞NF-κB的表达,了解NF-κB的活性,放免法检测TNF-α、IL-1的表达。结果:经中心静脉途径导入腺病毒转载的IκB基因,可降低HIBD大鼠脑内NF-κB活性,IκB干预1d组和7d组与HIBD损伤1d组和HIBD损伤7d组比较,NF-κB活性明显减少(P<0.05);降低脑内TNF-α、IL-1含量,IκB干预1d组和7d组与HIBD损伤1d组和7d组比较,TNF-α、IL-1含量明显减少(P<0.05)。结论:通过中心静脉途径注入腺病毒转载的IκB基因,直接增加脑内IκB的表达,阻断炎症因子TNF-α的合成,机制可能与其抑制了NF-κB的活性有关。
Objective :To explore the effect of inflammation reaction of HIBD rat model by infusing IκB gene into the rat model with adenovirus vector through the central vein. Methods:Forty rats were randomly divided into five groups:Group Ⅰ (control group) ,Group Ⅱ (HIBD 1d),Group Ⅲ (HIBD 7d),Group Ⅳ (Ad IκB therapy ld) ,and Group V (Ad IκB therapy 7d). The expression of NF--κB in the brain tisse was measured by Western--blot method. The levels of TNF--α and IL--1 in the brain tisse were recorded after injection at day 1 and 7. Results:After infusing IκB gene-- tansported-- adenovirus through central vein, the NF--κB expression in IκB therapy at day 1 and IκB therapy at day 7 was significantly lowered in comparison with that in HIBD ld group and HIBD 7d group, and the cytokine level was significantly reduced (P 〈 0.05) . Conclusion :It may be a new direction for therapy HIBD by increasing expression of IκB gene by infusing IκB gene-- tansported-- adenovirus through the central vein, and the possible neuroprotection mechanism of HIBD may be related to the activity of NF--κB.
出处
《黑龙江医药科学》
2008年第3期6-7,共2页
Heilongjiang Medicine and Pharmacy