川芎嗪注射液对急性脑梗死患者血清sCD40L及hs—CRP水平的影响

目的：观察川芎嗪注射液对急性脑梗死患者血清可溶性CD40配体（sCD40L）及超敏C-反应蛋白（hs-CRP）水平的影响。方法：采用随机对照的方法，将78例急性脑梗死患者随机分成治疗组和对照组，每组39例。所有患者均采用西医常规方法进行治疗，治疗组患者在此基础上加用川芎嗪注射液治疗，疗程为14d。评价两组患者的临床疗效及神经功能缺损评分，观察治疗前后两组患者血清sCD40L和hs—CRP水平的变化。结果：治疗后，治疗组和对照组的总有效率分别为92．31％和74．36％，治疗组的疗效优于对照组（P〈0．05）。治疗后，两组患者的血清sCD40L及hs—CRP水平均显著降低（P〈0．01），且治疗组患者的血清sCD40L及hs—CRP水平均低于对照组（P〈0．05）；治疗组患者的神经功能缺损评分显著降低（P〈0．01），且治疗组患者的评分低于对照组（P〈0．05）。结论：川芎嗪注射液治疗急性脑梗死具有较好的疗效，其机制可能与干扰脑缺血后血小板CD40／CD40L信号通路、抑制血小板活化、减轻炎症损伤有关。

Influence of Ligustrazine Injection on Levels of sCD40L and hs-CRP in Blood Serum of Patients with Acute Cerebral Infarction

Objective ： To observe the influence of Iigustrazine injection on the levels of soluble CD40 ligand （ sCD40L） and high sensitivity C-reactive protein （ hs-CRP） in blood serum of patients with acute cerebral infarction. Methods ： Seventy- eight patients with acute cerebral infarction were randomly divided into treatment group and control group with 39 cases in each group. AU the patients were treated by conventional western medicine therapy, and in addition the patients in the treatment group were treated with ligustrazine injection, with a course of 14 days. The clinical effect and the neurological deficit score were evaluated, and the levels of sCD40L and hs-CRP were detected. Results ： The total effective rates of treatment group and control group were 92. 31% and 74. 36% respectively, with statistical difference between two groups （ P 〈 0. 05 ） . After treatment, the levels of sCD40L and hs-CRP were decreased obviously in both groups （P 〈0.01）,and the levels of sCD40L and hs-CRP in treatment group were lower than those in control group （P 〈0. 05） ; the neurological deficit scores of treatment group were significantly decreased （P〈 0. 01 ）,and the scores of treatment group were lower than those of control group （P 〈0.05）. Conclusion： Ligustrazine injection has good effect in treating acute cerebral infarction, and its mechanisms may have relationship with interfering with the platelet CD40/CD40L signaling pathway after cerebral ischemia, inhibiting the platelet activation and alleviating the injury of inflammation.