CAJ | 학술논문

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20 m g ，连用6个月。在治疗前及治疗后28 d、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（IM T ）。结果与治疗前及对照组同期相比较，治疗组28 d、6个月 A PN 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28 d后2组颈动脉 IMT 均无明显变化；治疗6个月治疗组颈动脉 IM T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。
목적：연구아탁벌타정대뇌경사환자혈청중APN、Visfatin、TNF‐α화IL‐6수평급경동맥내‐중막후도（IMT）적영향，탐토아탁벌타정개대뇌경사환자경동맥죽양경화적치료궤제。방법118례합병경동맥죽양경화적뇌경사환자수궤분위대조조화치료조（아탁벌타정조）。제뇌경사상규치료외，치료조가용아탁벌타정，매만20 m g ，련용6개월。재치료전급치료후28 d、6개월시，추취정맥혈채용매련면역흡부시험법（ELASA）검측환자혈청중 APN、Visfatin、TNF‐α화IL‐6수평，경동맥초성검측경동맥내‐중막후도（IM T ）。결과여치료전급대조조동기상비교，치료조28 d、6개월 A PN 수평균승고， TNF‐α、IL‐6화Visfatin수평균하강，차이균유통계학의의。치료28 d후2조경동맥 IMT 균무명현변화；치료6개월치료조경동맥 IM T여치료전급대조조6개월상비균유현저성차이（ P＜0.05）。결론아탁벌타정장기응용가강저뇌경사환자경동맥 IMT ，기작용궤제제조지외환가능통과강저혈청중Visfatin、TNF‐α화IL‐6수평종이상조APN표체억제혈관염증。
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 atorvasta‐tin.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 (20 mg per night for 6 months)on the basis of control group. Serum APN ,TNF‐α,IL‐6 and Visfatin in venous blood were detected by ELASA and IM T by carotid ultrasonography before treatment and after 28‐day and 6‐month therapy.Results Compared before treat‐ment 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‐6 and Visfatin in the experiment group were signifi‐cantly lower than those in the control group (P<0.05). The carotid IMT in two groups showed no significant difference after 28‐day treatment ,which in the experiment group were significantly thinner than that in the control group(P<0.05). Conclu‐sion 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.