高脂血症兔主动脉NF-κB、VCAM-1和VEGF的表达及氟伐他汀的影响

目的观察高脂饮食后兔主动脉NF-κB、VCAM－1、VEGF的表达及氟伐他汀的影响，探讨高脂血症引起动脉粥样硬化可能的分子生物学机制和氟伐他汀的作用。方法健康雄性新西兰大耳白兔30只，随机分为5组，高脂饮食4周、6周、8周组，正常饮食和高脂饮食加氟伐他汀组。到规定时间点，处死动物取主动脉标本，观察组织形态学变化，用免疫组化的方法检查NF-κB、VCAM－1和VEGF的表达。结果①高脂血症可以引起NF-κB、VCAM－1、VEGF增加，与对照组比较差异有统计学意义（P〈0．01）。②LDL水平与NF-κB表达呈显著正相关（r=0．922，P〈0．01）；NF-κB与VCAM－1、VEGF呈显著正相关（r＝0．937，P〈0．01，r=0．894，P〈0．01）。③氟伐他汀可以减少NF-κB、VCAM－1和VEGF的表达（P＜0．05）。结论NF-κB、VCAM－1和VEGF参与了动脉粥样硬化的进程，炎症是高脂血症的伴随因素，引起了细胞增殖，与动脉粥样硬化密切相关：氟伐他汀可以减少其表达起到抗动脉粥样硬化作用。

Expression of NF-κB,VCAM-1 and VEGF in aorta of hyperlipemia rabbits and influence by Fluvastatin

Objective Observed expression of NF-κB,VCAM-1 and VEGF in aorta of hypedipemia rabbits to investigate probable inflammation nosogenesis of atherosclerosis and influence by Fluvastatin. Methods 24 healthy New Zealand rabbits were divided randomly into four group：high fat diet group 1 （4 weeks）,group 2 （6 weeks）,group 3 （8 weeks）, normal diet and high fat diet add Fluvastatin group. Animals were killed to obtain aorta tissue ,then observe morpholog change and expression of NF-κB,VCAM-1 ,VEGF by immunohistochemistry.Results （1）Hyperlipoidemia caused expression of NF-κB, VCAM-1 ,VEGF increased,which was highly difference with control group （P〈0.01）.（2）LDL level was positive correlation with expression of NF-κB（r=0.922 P〈0.01 ）,and NF-κB positive correlation with VCAM-1, VEGF（r=0.937,P〈0.01 ,r=0.894,P〈0.01 ）. （3）Fluvastatin decreased expressions of NF-κB,VCAM-1 ,VEGF（P〈0.05）.Condusion NF-κB, VCAM-1 ,VEGF participated process of atherosclerosis. This illustration that inflammation was accompaniment of hyperlipemia, which caused cell multiplication and intimate correlated with atherosclerosis.Fluvastatin decreased these expressions and had anti-atherosclerosis affect.