【作者】 周婷；

【导师】 丁美萍；

【作者基本信息】 浙江大学 ， 神经病学， 2008， 硕士

【摘要】 研究目的:本研究旨在通过测定急性脑梗死患者血清脂联素和IL-10水平,分析急性脑梗死患者血清脂联素与IL-10、脑梗死体积、NIHSS评分、血糖、血脂的相关性,为进一步探讨脑梗死的发生和发展提供一定临床理论依据。研究方法:1.研究对象脑梗死组动脉粥样硬化性脑梗死患者50例,男28例,女22例,年龄34～79岁,平均62.62±11.19岁。所有病例均符合2005年《中国脑血管病防治指南》制定的脑梗死诊断标准。并经头颅MRI证实为首发脑梗死患者。入选条件包括首次发病,在发病72h内入院。对照组健康体检者38例,男24例,女14例,年龄36～78岁,平均58.50±9.80岁。入组者均经头颅MRI检查无脑梗死。所有研究对象均排除糖尿病、肥胖(体重指数)25 kg/m~2)、心脏病、近期感染、肝肾疾病、周围血管闭塞性疾病、肿瘤、服用抗感染药物及(或)免疫抑制剂者、近期有外科手术和创伤史以及自身免疫性疾病。2.脂联素、IL-10检测:所有研究对象均禁食10h后于次日晨空腹采集静脉血4ml,放入不加抗凝剂的无菌离心管内,温室静置30min后,3000r/min离心15min,分离血清,低温冰箱-30℃保存备用。所有标本采集后一次性测定。人血清脂联素、IL-10测定采用ELISA试剂盒,试验步骤严格按照说明书进行操作。3、生化指标的测定:空腹血糖,血脂。4、体重指数(BMI)=体重(kg)/身高(m~2)、血压。5、计算脑梗死面积大小:参照按Pullicino公式计算梗死体积:脑梗死体积cm~3=长径×短径×梗死层面数/2。6、脑梗死患者入院当天进行神经功能评估:美国国立卫生研究院卒中量表评分(NIHSS评分)。7、统计学处理数据用SSPS11.0统计软件包进行分析。计量资料以均数±标准差((?)±s)或中位数和四分位数(25%,75%)表示;计数资料以百分位数(%)表示。根据数据类型采用t检验、t′检验或Mann-Whitney U-test。相关性分析采用Kendall’s tau_b。以p＜0.05为差异有统计学意义。研究结果:1.急性脑梗死组脂联素水平与正常对照组比较明显降低(中位数2.13mg/L对8.24mg/L,P＜0.01)。2.急性脑梗死组IL-10水平与正常对照组比较明显降低(中位数152.25pg/ml对574.32pg/ml,P＜0.01)。3.急性脑梗死组脂联素与IL-10呈正相关(r=0.274,P＜0.01),与低密度脂蛋白呈负相关(r=-0.252,P＜0.05),与高密度脂蛋白呈正相关(r=0.384,P＜0.05)。4.首次脑梗死后梗死体积与血浆脂联素成负相关(r=-0.201,P＜0.05);首次脑梗死后梗死体积与IL-10无明显相关性。血浆脂联素、IL-10水平与缺血性卒中神经功能评分均无明显相关性。研究结论:1.脑梗死的发生可能与脂联素等保护性抗炎因子的减少、血脂代谢紊乱有关,从而促进动脉粥样硬化,增加了脑梗死发生的危险。2.测定脂联素水平可作为判断脑梗死严重性的一个重要参考指标。更多还原

【Abstract】 Objective:In the present study we measured the serum levels of adiponectin and Interleukin-10(IL-10)in patients with acute cerebral infarction and analyze the relationship among adiponectin,IL-10,infarct volume,NIHSS score,levels of blood glucose and blood lipids.Methods:1.SubjectsCerebral infarction group:we examined 50 patients with atherosclerotic cerebral infarction.They were composed of 28 men and 22 women with the average age of 62.62±11.19 years(range 34-79 years).All included subjects were hospitalized within 72 hours after they were attacked by initial cerebral infarction.The diagnostic criteria of cerebral infarction was based on Chinese Guideline for Cerebrovascular Disease Prevention and Treatment(2005).They were diagnosed by head magnetic resonance imaging(MR1).Control group:38 subjects without clinical evidence of cerebral infarction and further confirmed by MRI scanning were recruited from an unselected population who underwent routine health checkups.There were 24 men and 14 women with the average of 58.50±9.8 years(range 36-78 years). Those subjects with diabetes,obesity(BMI＞25 kg/m~2),heart disease, evidence of recently infection,liver and/or kindey disease,peripheral vascular occlusive disease,tumor,taking anti,infective and/or immunosuppressive agents, history of recent surgery and/or trauma and those diagnosed with autoimmune disease were excluded2.Measurements of serum adiponectin and IL-10:Four ml of venous blood samples of all the subjects were drawn after 10 h overnight fast and kept with sterile centrifuge tube without anti-coagulant.Serum was separated by centrifugating the blood sample at 3000r/min for 15 min after clot at room temperature for 30 min.Serum samples were kept at -30℃for subsequent assay.The concentrations of serum adiponectin and IL-10 were determined by a commercial enzyme-linked immunosorbent assay(ELISA)kit according to the manual.3.Biochemical parameters measurements:fasting blood glucose,blood lipids.4.Anthropometric measurements:The body mass index(BMI)was calculated as weight/height~2(kg/m~2).Blood pressure was measured simultaneously.5.Calculation of the infart volume:Infarct volume was calculated according to the Pullicino formula based on the result of CT/MRI scanning(Infarction Volume=long diameter×short diameter×the Summing the thicknesses of infarct/2).6.Neurological functional assessments were conducted at the first day after admission according to the National Institutes of Health Stroke Scale(NIHSS).7.Statistical analysis:Statistical analysis was performed using ’SPSS’ v11.0.Measurement data were presented as means±standard deviation or median and quartile(25%,75%). Differences between these variables were assessed using t test or t′test.Numeration data are presented as quartile(%)with differences assessed using the Mann-Whimey U test.The degree of association between the measured variables was estimated using Kendall’s tau-b.P＜0.05 was considered statistically significant.Results:1.The serum level of adiponectin was significantly lower in subjects with acute cerebral infarction than that in the healthy controls(median 2.13mg/L vs 8.24mg/L,P＜0.01).2.The serum level of IL-10 was significantly lower in the group of patients with acute cerebral infarction than that in the control group(median 152.25pg/ml vs 574.32pg/ml,P＜0.01).3.The serum adiponectin level was positively correlated with IL-10(r=0.274, P＜0.01)and HDL cholesterol level(r=0.384,P＜0.05).In contrast,serum adiponectin concentration was negatively correlated with LDL cholesterol level(r=-0.252,P＜0.05).4.The initial infarct volume was negatively correlated the serum level of adiponectin(r=-0.201,P＜0.05).There was no significant correlation identified between infarct volume and the concentration of IL-10.Additionally,there was no significant correlation among the level of serum adiponectin,IL-10 and the NIHSS.Conclusion:1.The decreased anti-inflammatory cytokines,such as adiponectin,and lipid disorder may be related to the pathogenesis of cerebral infarction.They increased the risk of cerebral infarction by inducing atherosclerosis and thrombosis. 2.The serum concentration of adiponectin may serve as a significant marker of the severity of cerebral infarction.更多还原