摘要
目的观察脑梗死患者血清HMGB1、IL-17A和S-100A12水平的变化,并探讨瑞舒伐他汀钙治疗对脑梗死的脑保护作用机制。方法采用随机、对照、单盲法的前瞻性研究。根据颈动脉彩超检查结果,将卒中单元中符合纳入标准的280例急性脑梗死患者分为稳定斑块组100例和易损斑块组180例,后者按照随机数字法分为低剂量治疗组(A组,瑞舒伐他汀片,5 mg/晚,口服)和高剂量治疗组(B组,瑞舒伐他汀片,20 mg/晚,口服)各90例。检测发病第1天(治疗前)、第3天、第7天、第14天血清HMGB1、IL-17A和S-100A12水平;治疗前、治疗后第3天、治疗后1 w、2 w和3 w神经功能缺损采用NIHSS评分评定。结果发病第1天,易损斑块组(A组和B组)患者血清HMGB1、IL-17A和S-100A12水平高于稳定斑块组,且于第3天均达峰值,继之出现缓慢下降。在发病第7天、第14天B组血清HMGB1、IL-17A和S-100A12含量均明显低于A组(均P<0.01)。治疗后第3天,A组和B组患者NIHSS评分较治疗前明显增加,达峰值(均P<0.01)。治疗后2 w和3 w,B组患者NIHSS评分低于A组(均P<0.01)。易损斑块组患者血清S-100A12水平与NIHSS评分呈正相关(发病第1天,分别r1=0.856,发病第3天,r1=0.870,均P<0.01)。此外,血清HMGB1和IL-17A水平呈显著正相关(发病第1天,r=0.972,发病第3天,r=0.975,均P<0.01)。结论血清S-100A12浓度可作为评估脑梗死后神经功能损伤严重程度的血清学指标,可作为评估颈动脉斑块易损性的血清学指标,HMGB1和IL-17A可能参与了脑梗死后急性期炎性反应过程。采取高强度他汀治疗具有减轻脑梗死后继发炎症反应、保护脑细胞和提高患者神经功能的作用。
Objective To observe the changes of high mobility group box-1（ HMGB1） and interieukin-17A（ IL-17A） and Ca-binding protein A12（ S-100A12） in patients with acute cerebral infarction（ ACI）,and to explore the probablely protective mechanism of Rosuvastatin. Methods According to the results of carotid artery ultrasound,280 patients with ACI were divided into carotid stable plaque group（ n = 100） and carotid vulnerable plaque group（ n = 180）. 180 cases with carotid vulnerable plaque were randomly divided into low-dose group（ A group,n = 90,rosuvastatin 5 mg / d,oral） and highdose group（ B group,n = 90,rosuvastatin 20 mg / d,oral）. The therapeutic course for all was 3 weeks. Plasma samples were obtained at the 1st day（ before treatment）,on days 3,7 and 14 of onset. Levels of serum HMGB1,IL-17 A and S-100A12 were measured by enzyme-linked immunosorbent assay. Before treatment,on the 3rd day,in 1 weeks,2 weeks and 3 weeks after treatment,the neurological deficits evaluated by National Institute of Health stroke scale（ NIHSS）. Results Compared with carotid stable plaque group,levels of HMGB1,IL-17 A and S-100A12 in A group and B group were significantly increased on the first day of illness（ all P〈 0. 01）,peaked at 3rd day,decreased gradually thereafter. Plasma HMGB1,IL-17 A and S-100A12 levels in B group were significantly lower than that in A group at 7d and 14d（ all P〈 0. 01）. On days3,the NIHSS scores were reached the peak,and obviously higher than that before treatment（ all P 〈0. 01）. Compared with A group,the NIHSS scores in B group after the 2nd and 3rd week were significantly decreased（ all P 〈0. 01）. Plasma levels of S-100A12 in A group and B group were positively correlated with NIHSS scores（ at the 1st day,r = 0. 856,on the 3rd day,r = 0. 870,all P 〈0. 01）. In addition,serum HMGB1 levels in patients with ACI were markedly positively relevant to serum IL-17 A levels（ before treatment,r = 0. 972,at 3rd day,r = 0. 975,all P〈 0. 01）. Conclus
出处
《中风与神经疾病杂志》
CAS
北大核心
2016年第2期109-112,共4页
Journal of Apoplexy and Nervous Diseases
基金
武汉市卫生局科研资助项目(No.WX10C23)
