| 谭峰,顾卫,黄涛,王金良,吴海科,黄彪.清开灵注射液对急性脑梗死患者血小板CD62P与细胞因子的影响[J].中国中西医结合杂志,2003,(3):195-197 |
| 清开灵注射液对急性脑梗死患者血小板CD62P与细胞因子的影响 |
| Effect of Qingkailing Injection on Platelet CD62P and Cytokines in Patients with Acute Cerebral Infarction |
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| DOI： |
| 中文关键词: 清开灵注射液 急性脑梗死 血小板CD62P 细胞因子 |
| 英文关键词:Qingkailing Injection acute cerebral infarction platelet CD62P cytokines |
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| 中文摘要: |
| 目的:观察清开灵注射液对急性脑梗死(ACI)患者的临床疗效及血小板 CD62P阳性表达率与细胞因子含量动态变化的影响。方法:65例发病在 3天以内的 ACI患者随机分为两组,治疗组用清开灵注射液和低分子右旋糖研治疗,对照组用低分子右旋糖研治疗。采用流式细胞仪(FCM)、电化学发光(EC)等技术测定两组 ACI患者治疗前后血小板 CD62P的阳性表达率与肿瘤坏死因子a(TNF-α)、白细胞介素-2受体(IL-2R),白细胞介素一6(IL.6)等指标的水平,并以3O例健康人作正常对照及相关分析。结果:ACI患者治疗前后CD62P、TNF-a、I丁ZR、IL-6水平均显著高于健康人组(P<0.05或P<0.01),ACI患者CD62P表达与 TNF-a、IL-ZR二L-6水平升高呈正相关;治疗组治疗后 CD62P、TNF.a、IL.ZR、IL-6水平的降低较对照组显著(P<0.05),临床治愈率、显效率亦明显高于对照组(P<0.05)。结论:清开灵注射液治疗ACI的作用机制与其抑制血小板活化增强、减轻细胞因子介导的中枢神经系统免疫应答及炎症损伤等有关。 |
| 英文摘要: |
| Objective; To study the therapeutic effect of Qingkailing Injection (QKL) for acute cerebral infarction (ACI) and its influence on platelet CD62P expression and cytokines contents in peripheral blood in patients. Methods: Sixty-five patients of ACI with in the first 72 hrs after onset were randomly divided into treated group (treated with QKL and low molecular dextran) and the control group (treated with low molecular dextran alone). Another group of 30 healthy adults was set up for normal control. Platelet CD62P expression was measured by flow cytometry and the levels of tumor necrosis factor a( TNF-α), interleukin-2 receptor (IL-2R) and interleukin-6 (IL-6) were measured by electrochemoluminescence (ECL) before and after treatment. Results: Levels of CD62P, TNF-α, IL-2R and IL-6 in the ACI patients, either before or after treatment, were all obviously higher than those in the normal control group (P<0.01 or P<0.05), the elevation of CD62P expression was positively related with the elevation of the TNF-α, IL-2R and IL-6. After treatment, all the criteria tested decreased more significantly in the treated group after treatment than those in the control group ( P < 0.05), and the clinical cure rate and markedly effective rate were also higher in the former than those in the latter ( P < 0.05). Conclusion: The mechanism of QKL in treating ACI is related with its actions in inhibiting platelet activation, reducing the cytokines mediated immune response of central nerve system and eliminating inflammatory injury. |
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