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普伐他汀对缺血性脑卒中患者血脂和血浆炎症因子的影响

     

摘要

目的:探讨普伐他汀对缺血性脑卒中患者血脂和血浆炎症因子的影响.方法:选择2007年1月-2010年12月在我院住院的80例缺血性脑卒中患者,随机均分为对照组和普伐他汀组.2组患者均给予常规对症治疗.普伐他汀组在此基础上加用普伐他汀10 mg,qd,连用4周.比较2组治疗前后的血清胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、血浆超敏C反应蛋白(hs-CRP)、基质金属蛋白9(MMP-9)和神经功能缺损评分的变化.结果:治疗4周后,普伐他汀组TC、TG和LDL-C水平较治疗前明显下降,HDL-C水平明显上升(P<0.05);而对照组治疗前、后比较差异均无统计学意义(P>0.05).2组治疗后,TC、TG、LDL-C、HDL-C水平比较,差异均有统计学意义(P<0.05),普伐他汀组明显优于对照组.2组血浆hs-CRP、MMP-9和神经功能缺损评分水平均较治疗前明显下降(P<0.05或P<0.01),但普伐他汀组比对照组下降更明显(P<0.05).结论:普伐他汀治疗缺血性脑卒中的疗效确切,其作用机制可能通过降低血脂、减轻炎症反应,以改善动脉粥样硬化,改善卒中部位缺血缺氧和缺损神经功能.%OBJECTIVE: To investigate the effects of pravastatin on blood lipid and plasma inflammatory cytokines in patients with ischemic stroke. METHODS: 80 hospitalized patients with ischemic stroke were randomly divided into control group and pravastatin group. All patients were given nifedipine appropriately to control hypertension, mannitol to control intracranial pressure, cerebrolysin to nourish brain cells, aspilin anticoagulation and other symptomatic treatment. Pravastatin group were additionally given pravastatin 10 mg, qd for 4 weeks. The changes of TC, TG, LDL-C, HDL-C, hs-CRP, MMP-9 and neurologic impairment scores were compared between 2 groups, and clinical efficacy was also evaluated. RESULTS: After 4 weeks of treatment, TC, TG and LDL-C levels decreased significantly, compared with before treatment. HDL-C levels were significantly increased in pravastatin group (P<0.05). There were no statistically differences in control group before and after treatment (P>0.05); Plasma hs-CRP and MMP-9 levels decreased significantly, compared with before treatment (P<0.05 orP<0.01), and the decrease of them in pravastatin group were more significant than in control group (P<0.05); the neurological deficit scores of two groups were significantly decreased, compared with before treatment (P<0.01 or P<0.05), and the decrease of it in pravastatin group was more significant than control group (P<0.05). CONCLUSIONS: Treatment of ischemic stroke with pravastatin is effective, and its mechanism may be associated with decreasing blood lipid, reducing inflammation, improving atherosclerosis, then resulting in the improvement of ischemia and hypoxia and defects of neurological function.

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