中国医师进修杂志
中國醫師進脩雜誌
중국의사진수잡지
CHINESE JOURNAL OF POSTGRADUATES OF MEDICINE
2009年
10期
15-18
,共4页
刘坤%宫珍卿%王永久%胡新建%毕仕强%臧艳平
劉坤%宮珍卿%王永久%鬍新建%畢仕彊%臧豔平
류곤%궁진경%왕영구%호신건%필사강%장염평
肿瘤坏死因子α%C反应蛋白质%脑梗塞%阿托伐他汀钙
腫瘤壞死因子α%C反應蛋白質%腦梗塞%阿託伐他汀鈣
종류배사인자α%C반응단백질%뇌경새%아탁벌타정개
Tumor necrosis factor alpha%C-reactive protein%Cerebral infarction%Atorvastatin calcium
目的 观察阿托伐他汀钙对急性脑梗死患者血清C反应蛋白(CRP)和肿瘤坏死因子(TNF)-α水平的影响,探讨阿托伐他汀钙抑制急性脑缺血后炎性损伤的机制.方法 选择发病24h内住院的急性脑梗死患者84例,随机分为阿托伐他汀钙治疗组(A组)和常规治疗组(B组),每组各42例.两组均应用抗血小板和改善脑血液循环药物等常规治疗,A组在此基础上口服阿托伐他汀钙20 mg/d,连续治疗28 d.于治疗前及治疗后3、7 d检测两组患者血清CRP和,TNF-α水平,并比较两组患者欧洲卒中量表(ESS)评分的差异.另选择同期健康体检者16例作为健康对照组(C组).结果 84例急性脑梗死患者发病后血清TNF-α和CRP水平显著升高(P<0.01或<0.05),其中CRP在治疗后3d达高峰,TNF-α在治疗后7d达高峰.A组峰值均低于B组[(13.00±2.45)mg/L比(19.21±3.67)mg/L,(19.79±11.01)ng/L比(30.69±18.47)ng/L,P<0.05].治疗后7 d A组ESS评分高于B组[(79.19±30.59)分比(63.91±27.87)分],差异有统计学意义(P<0.05).结论 阿托伐他汀钙可通过降低血清CRP和TNF-α水平而抑制急性脑缺血后炎性损伤,具有降脂以外的神经保护作用.
目的 觀察阿託伐他汀鈣對急性腦梗死患者血清C反應蛋白(CRP)和腫瘤壞死因子(TNF)-α水平的影響,探討阿託伐他汀鈣抑製急性腦缺血後炎性損傷的機製.方法 選擇髮病24h內住院的急性腦梗死患者84例,隨機分為阿託伐他汀鈣治療組(A組)和常規治療組(B組),每組各42例.兩組均應用抗血小闆和改善腦血液循環藥物等常規治療,A組在此基礎上口服阿託伐他汀鈣20 mg/d,連續治療28 d.于治療前及治療後3、7 d檢測兩組患者血清CRP和,TNF-α水平,併比較兩組患者歐洲卒中量錶(ESS)評分的差異.另選擇同期健康體檢者16例作為健康對照組(C組).結果 84例急性腦梗死患者髮病後血清TNF-α和CRP水平顯著升高(P<0.01或<0.05),其中CRP在治療後3d達高峰,TNF-α在治療後7d達高峰.A組峰值均低于B組[(13.00±2.45)mg/L比(19.21±3.67)mg/L,(19.79±11.01)ng/L比(30.69±18.47)ng/L,P<0.05].治療後7 d A組ESS評分高于B組[(79.19±30.59)分比(63.91±27.87)分],差異有統計學意義(P<0.05).結論 阿託伐他汀鈣可通過降低血清CRP和TNF-α水平而抑製急性腦缺血後炎性損傷,具有降脂以外的神經保護作用.
목적 관찰아탁벌타정개대급성뇌경사환자혈청C반응단백(CRP)화종류배사인자(TNF)-α수평적영향,탐토아탁벌타정개억제급성뇌결혈후염성손상적궤제.방법 선택발병24h내주원적급성뇌경사환자84례,수궤분위아탁벌타정개치료조(A조)화상규치료조(B조),매조각42례.량조균응용항혈소판화개선뇌혈액순배약물등상규치료,A조재차기출상구복아탁벌타정개20 mg/d,련속치료28 d.우치료전급치료후3、7 d검측량조환자혈청CRP화,TNF-α수평,병비교량조환자구주졸중량표(ESS)평분적차이.령선택동기건강체검자16례작위건강대조조(C조).결과 84례급성뇌경사환자발병후혈청TNF-α화CRP수평현저승고(P<0.01혹<0.05),기중CRP재치료후3d체고봉,TNF-α재치료후7d체고봉.A조봉치균저우B조[(13.00±2.45)mg/L비(19.21±3.67)mg/L,(19.79±11.01)ng/L비(30.69±18.47)ng/L,P<0.05].치료후7 d A조ESS평분고우B조[(79.19±30.59)분비(63.91±27.87)분],차이유통계학의의(P<0.05).결론 아탁벌타정개가통과강저혈청CRP화TNF-α수평이억제급성뇌결혈후염성손상,구유강지이외적신경보호작용.
Objective To observe the effects of atorvastatin calcium on serum tumor necrosis factor alpha (TNF)-α and C-reactive protein (CRP) in patients with acute cerebral infarction (ACI), so as to approach the mechanism of atorvastatin calcium inhibiting ACI inflammatory injury. Methods Eighty-four patients with ACI were randomly divided into 2 groups: group B (42 cases, treated with antiplatelet therapy and improving cerebral circulation), group A(42 cases, treated with atorvastatin calcium 20 mg/d after the onset of ACI for 28 days on the base of group B). TNF- α and CRP were detected before treatment and in the 3rd,7th day after treatment. The European stroke scale (ESS) was evaluated on the same time. A healthy control group (group C, 16 cases) was also included in the study. Results The peak of CRP and TNF-α levels were observed in the 3rd and 7th day after treatment respectively, and the levels of group A were lower than those of group B [(13.00 ± 2.45) mg/L vs (19.21 ± 3.67) mg/L,(19.79 ± 11.01) ng/L vs (30.69 ± 18.47) ng/L, P < 0.05]. In the 7th day after treatment, the scores of ESS was higher in group A than that in group B [(79.19 ± 30.59) scores vs (63.91 ± 27.87) scores, P < 0.05]. Conclusions Atorvastatin calcium can prevent the increase of serum TNF-α and CRP, and it has anti-inflammatory effect. Atorvastatin calcium may have the role of neuroprotection besides lipid-lowering.