丁苯酞对急性脑梗死患者血清白介素-6及超敏CRP的影响

发布时间：2018-06-18 05:53

本文选题：丁苯酞 + 急性脑梗塞　；参考：《河北医科大学》2017年硕士论文

【摘要】：目的:人类死亡的诱发因素中,脑血管病位居前2位。相较于西方国家,国内脑血管病的患病人数以及死亡人数均要比心血管病多出很多。缺血性脑血管病,患病率相对偏高,并能够诱发神经元受损。缺血形成阶段中,神经元受损需经历多个环节和步骤,如自由基受损、谷氨酸的释放及其毒性作用、细胞中的钙含量增多以及炎症级联作用等。这些年,我们将自由基氧化、炎症级联两种反应及其诱发的继发性脑损伤,纳入研究行列。国内外研究发现丁苯酞可以对不同的病理环节起作用,从而被视作治疗急性缺血性脑卒中的一类新药物。缺血性卒中演变进程中,丁苯酞可以抑制和缓解脑组织损伤,使脑组织恢复正常或接近正常的供血状态。动物实验早已证实:丁苯酞可明显缩小急性脑梗死大鼠脑细胞死亡的实际面积,缓解脑水肿,调节脑细胞异常的能量代谢,促进侧枝循环和正常的血流量;对神经细胞的快速凋亡起抑制作用,同时也可以对抗血栓形成,避免血小板大量地聚集。但是对脑梗死后的炎症反应影响报道不多。本研究旨在对急性脑缺血病例给予丁苯酞,观察用药前后白介素6(IL-6)以及超敏CRP两项指标的变化,探讨神经功能缺损程度和IL-6之间的关系,为丁苯酞治疗急性脑梗塞的机制提供更多地理论依据。方法:选择发病时间48h的急性脑梗死病例共60例。对所有病例进行随机分组,一组为治疗组(30例),另一组为对照组(30例);另选择20名正常体检者,设为正常组。急性脑梗死对照组病例接受常规疗法,如阿司匹林、他汀类稳定斑块,辅助降压以及降血糖及对症等多种治疗措施。治疗组:以对照组用药基础上,加用丁苯酞氯化钠注射液,剂量为100m1/次,静脉滴注,2次/日;滴注时间50-70min;两次静滴时间间隔6h,对丁苯酞注射液进行输注时,需选择非PVC输液器。全部病例的疗程为14d;14天后给予口服丁苯酞软胶囊,200mg/次,3次/日,持续30d.两组患者均于住院当天(第1d),治疗后第7,14以及30d四个时段,参照美国卫生研究院卒中量表(The national institutes of health stroke scale NIHSS)以及自理能力Barthel指数(BI)对两组病例进行评分。同时,对两组病例治疗前后不同时段的超敏CRP和IL-6水平分别进行检测,分析神经功能缺损严重性和超敏CRP以及IL-6指标存在的关联。结果:1神经功能损伤程度评分,在治疗前,治疗组和对照组无明显差异;治疗后,两组的评分均较治疗前有明显改善,且其中治疗组治疗后的评分较前改善更为显著(P0.05)。2超敏CRP和IL-6水平:治疗组和对照组病例的超敏CRP和IL-6水平均显著高于正常组,有统计学差异(P0.05);治疗第7、14、30d,治疗组和对照组患者血清超敏CRP和IL-6水平均低于治疗前,且治疗组病例的超敏CRP和IL-6检测值的降低程度要高于对照组,有统计学差异(P0.05)。3针对急性脑梗死病例,NIHSS、BI评分和sCRP以及IL-6水平之间呈显著正相关(P0.05)。结论:1急性脑梗死患者NIHSS、BI评分和sCRP以及IL-6水平之间呈显著正相关;2给予丁苯酞能显著改善急性脑梗死患者神经功能缺损程度;3下调sCRP、IL-6水平可能是丁苯酞发挥神经保护作用的机制之一。
[Abstract]:Objective: of the leading factors of human death, cerebrovascular disease is the top 2. Compared with the western countries, the number of patients with cerebrovascular disease and the number of deaths are much more than cardiovascular disease. Ischemic cerebrovascular disease, the incidence of disease is relatively high, and can induce neuron damage. In the ischemic formation stage, neuron damage needs to experience a lot. Links and steps, such as free radical damage, the release of glutamic acid and its toxic effects, increased calcium content in cells and cascade of inflammation, we have included free radical oxidation, two reactions and induced secondary brain damage in these years. Domestic and foreign studies have found that butylphthalide can be used for different pathological links. It is considered as a new drug for the treatment of acute ischemic stroke. In the course of the evolution of ischemic stroke, butylphthalide can inhibit and alleviate brain tissue damage, make the brain restore normal or close to normal blood supply. Animal experiments have already proved that butylphthalide can significantly reduce the death of brain cells in rats with acute cerebral infarction The area, which alleviates brain edema, regulates the energy metabolism of abnormal brain cells, promotes the collateral circulation and normal blood flow, inhibits the rapid apoptosis of the nerve cells, and can also antagonize the formation of thrombus and avoid massive aggregation of platelets. However, there are few reports on the effect of the inflammatory reaction after cerebral infarction. This study aims at acute brain deficiency. The changes in the two indexes of interleukin 6 (IL-6) and hypersensitivity CRP were observed in the blood cases, and the relationship between the degree of nerve function defect and IL-6 was explored, and more theoretical basis was provided for the mechanism of butylphthalide in the treatment of acute cerebral infarction. Methods: 60 cases of acute cerebral infarction were selected at the time of the onset of 48h. The treatment group (30 cases), the other group was the control group (30 cases), and the other 20 normal subjects were selected as the normal group. The patients in the control group of acute cerebral infarction were treated with conventional therapy, such as aspirin, statin stable plaque, auxiliary antihypertensive and hypoglycemic and symptomatic treatment. The treatment group was based on the control group. With Butylphthalide and Sodium Chloride Injection, dosage of 100m1/, intravenous drip, 2 times / day, infusion time 50-70min and two time interval 6h, non PVC infusion apparatus should be selected when infusion of butylphthalide injection. The course of all cases is 14d; 14 days after 14 days, oral Butylphthalide Soft Capsules, 200mg/ times, and 3 / day, continuous 30D. two groups are all On the day of hospitalization (1D), at the four periods of 7,14 and 30d after treatment, the two groups were evaluated with reference to the apoplexy of the US Institutes of Health (The National Institutes of Health Stroke Scale NIHSS) and the self-care capacity Barthel index. The correlation between the severity of nerve function defect and the hypersensitivity CRP and the IL-6 index was analyzed. Results: there was no significant difference between the treatment group and the control group before the treatment. The score of the 1 nerve function damage degree was no significant difference before the treatment. The scores of the two groups were significantly improved after the treatment, and the scores of the treatment group were more significant than those before the treatment (P0.05). .2 hypersensitivity CRP and IL-6 level: the hypersensitivity CRP and IL-6 water in the treatment group and the control group were significantly higher than the normal group, with a statistically significant difference (P0.05). The serum hypersensitivity CRP and IL-6 water in the treatment group and the control group were lower than before the treatment, and the degree of hypersensitivity CRP and IL-6 detection in the treatment group was higher than that of the control group. There was a significant positive correlation between NIHSS, BI score and sCRP and IL-6 levels (P0.05) for acute cerebral infarction (P0.05). Conclusion: 1 there was a significant positive correlation between NIHSS, BI score and sCRP and IL-6 levels in patients with acute cerebral infarction; 2 the degree of neurological impairment in patients with acute cerebral infarction was significantly improved; 3 The level of sCRP and IL-6 may be one of the mechanisms of neuroprotective effect of butylphthalide.
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R743.3

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