阿托伐他汀对急性脑梗死患者炎性细胞因子及神经功能缺损的影响

目的 观察阿托伐他汀对急性脑梗死患者神经功能缺损及血清高敏C反应蛋白(hs-CRP)、白细胞介素6(IL-6)、IL-10及内皮素1(ET-1)的影响.方法 采用随机数字表法将首次发生脑梗死的86例患者分为阿托伐他汀组(43例)和常规对照组(43例).常规对照组给予常规治疗；阿托伐他汀组在常规治疗基础上给予阿托伐他汀10 mg,1次/d,口服.分别于人院后第1天、治疗30d时清晨空腹抽血检测血清hs-CRP、IL-6、IL-10及ET-1水平；发病3个月时进行神经功能缺损评分美国国立卫生研究院卒中量表(NIHSS)评分]和Barthel指数评分.结果 治疗30 d时,阿托伐他汀组和常规治疗组血清hs-CRP、IL-6、ET-1均明显低于治疗前阿托伐他汀组:(7.4±2.6) mg/L比(12.1±5.3)mg/L,(9.4±1.8) μg/L比(20.3±6.8) μg/L,(68±16) μg/L比(89±20) μg/L,常规治疗组:(9.4±3.6) mg/L比(13.4±4.8)mg/L,(15.4±4.6)μg/L比(22.7±6.7) μg/L,(84±19) μg/L比(92±21) μg/L],IL-10明显高于治疗前阿托伐他汀组:(9.4±3.1)μg/L比(3.1±0.5)μg/L；常规治疗组:(4.6±1.8) μg/L比(2.7±0.4)μg/L],差异均有统计学意义(均P＜0.01).治疗30d时,阿托伐他汀组血清hs-CRP、IL-6、ET-1明显降低于而IL-10明显高于常规治疗组(均P＜0.01).发病后3个月,阿托伐他汀组和常规治疗组NIHSS评分较本组治疗前明显降低分别为(2.0±1.7)分比(4.2±2.3)分,(2.5±1.9)分比(4.3±2.2)分],Barthel指数得分明显增高分别为(95±6)分比(50±10)分,(95±8)分比(58±12)分],差异均有统计学意义(均P＜0.01)；治疗后阿托伐他汀组和常规治疗组NIHSS评分及Barthel指数得分比较,差异无统计学意义(P＞0.05).结论 阿托伐他汀有明确不依赖调脂的脑保护作用,有助于脑梗死后神经功能恢复,可以提高动脉粥样硬化斑块稳定性,具有抗粥样硬化作用.

Refluence of atorvastatin statins on inflanunatory cytokine and nerve function defect of patients with acutecerebral infarction

Objective To observe the refluence of atorvastatin statins on sermn levels of high sensitivity C reaction protein （hs-CRP）, interleukin （IL）-6, IL-10, endothelin-1 （ET-1） and the nerve function defect of patients with acute cerebral infarctiorL Methods All 86 patients with acute cerebral infarction for the first time were randomly divided into atorvastatin group （43 cases） and control group （43 cases）, The control group received conventional therapy and the atorvastatin group received atorvastatin 10 mg/d on the basis of conventional therapy. The course of treatment was 30 days. In the first day of hospitalization and after treatment for 30 days, serum hs-CRP, IL-6, IL-10 and ET-lvalue were detected respectively, and the National Insititute of Health Stroke Scale （NIHSS） score and Barthel index scores were performed. Results Compared to before treatment, serum hs-CRP and IL45 significantly decreased in atorvastatin group and control group after treatment for 30 days atorvastatin group ： （ 7. 4 ± 2. 6 ） mg/L vs （ 12. 1± 5. 3 ） mg/L, （9. 4 ± 1.8）μg/L vs（20. 3 ±6. 8）μg/;control group： （9.4 ±3. 6） mg/L vs（13.4 ±4. 8）mg/L, （15.4 ±4.6） μg/L vs （22. 7 ± 6. 7） μg/L ], IL-10 increased significantly atorvastatin group： （ 9. 4 ± 3. 1 ） μg/L vs （ 3. 1 ± 0. 5 ） μg/L ; control group： （4. 6 ±1.8）μg/L vs（2.7 ±0.4）μg/L], and ET-1 decreased atorvastatin group： （68 ± 16） μg/L vs（89 ±20）μg/L; control group：（84 ±19）μg/L vs（92 ±21）μg/L], and there were significant differences（all P 〈0.01）. 30 days after treatment, compared with the control group, the levels of hs-CRP, IL-6, ET-1 in atorvastatin group decreased, IL-10 increased （all P 〈0. 01 ）. Three months after onset, compared to before treatment, the scores of NIHSS in atorvastatin group and control group decreased （2. 0± 1.7 ） scores vs （4. 2± 2. 3 ） scores, （ 2. 5± 1.9 ） scores vs （ 4. 3±2. 2 ） scores, respectively], and the scores of Barthel index increased （95 ±6）scores vs （50± 10）scores, （95 ± 8 ）scores vs （58 ±12） scores ] （all P 〈 0. 01 ）. Compared with control group, there was no significant difference in NIHSS scores and Barthel index scores in atorvastatin group（all P 〉 0. 05）. Conclusion Atorvastatin have cerebral protective effects, which can help the recovery of nerve function after cerebral infarction and can improve atherosclerotic Dlanue stability.