阿托伐他汀钙治疗脑梗死患者颈动脉粥样硬化的机制探讨

Study on mechanism of carotid atherosclerosis in patients with cerebral infarction treated with atorvastatin calcium

目的研究阿托伐他汀对脑梗死患者血清中APN、Visfatin、TNF-α和IL-6水平及颈动脉内-中膜厚度(IMT)的影响,探讨阿托伐他汀钙对脑梗死患者颈动脉粥样硬化的治疗机制。方法 118例合并颈动脉粥样硬化的脑梗死患者随机分为对照组和治疗组(阿托伐他汀组)。除脑梗死常规治疗外,治疗组加用阿托伐他汀,每晚20mg,连用6个月。在治疗前及治疗后28d、6个月时,抽取静脉血采用酶联免疫吸附试验法(ELASA)检测患者血清中APN、Visfatin、TNF-α和IL-6水平,颈动脉超声检测颈动脉内-中膜厚度(IMT)。结果与治疗前及对照组同期相比较,治疗组28d、6个月APN水平均升高,TNF-α、IL-6和Visfatin水平均下降,差异均有统计学意义。治疗28d后2组颈动脉IMT均无明显变化;治疗6个月治疗组颈动脉IMT与治疗前及对照组6个月相比均有显著性差异(P<0.05)。结论阿托伐他汀长期应用可降低脑梗死患者颈动脉IMT,其作用机制除调脂外还可能通过降低血清中Visfatin、TNF-α和IL-6水平从而上调APN表达抑制血管炎症。

Objective To study the levels of serum APN,TNF-α,IL-6,Visfatin and the effect on intimal media thickness（IMT）in patients with cerebral infarction treated with atorvastatin,and to explore treatment mechanism of atorvastatin.Methods 118 cases were randomly divided into two groups：the control group and the experiment group（atorvastatin group）.The control group received routine therapy.The treatment in experiment group added atorvastatin（20mg per night for 6months）on the basis of control group.Serum APN,TNF-α,IL-6and Visfatin in venous blood were detected by ELASA and IMT by carotid ultrasonography before treatment and after 28-day and 6-month therapy.Results Compared before treatment with after 28-day and 6-month therapy,the levels of serum APN in the experiment group were significantly higher than those in the control group（P〈0.05）.And the levels of serum TNF-α,IL-6and Visfatin in the experiment group were significantly lower than those in the control group（P〈0.05）.The carotid IMT in two groups showed no significant difference after28-day treatment,which in the experiment group were significantly thinner than that in the control group（P〈0.05）.Conclusion Long-term usage of atorvastatin could lower the thickness of carotid atherosclerosis.Except for regulating lipid,the mechanism may up-regulate APN expression to inhibit vascular inflammatory by reducing the levels of serum Visfatin,TNF-αand IL-6.