摘要
目的 探讨依达拉奉治疗急性脑梗死的临床疗效和作用机制。方法 选择2011年3月-2013年3月就诊于中国医科大学附属第一医院的急性脑梗死患者121例,随机分为对照组(60例)和治疗组(61例)。对照组采用常规治疗,治疗组加用依达拉奉注射液10 mg/次,加入0.9%氯化钠溶液100 mL,静脉滴注,2次/d,10 d为1个疗程。治疗1~2个疗程后比较两组治疗前,治疗5、10 d,治疗结束时神经功能缺损(NIHSS)评分、促炎/抑炎细胞因子、自由基的情况。结果 治疗组和对照组治疗的有效率分别是83.61%、61.67%,两组比较差异有统计学意义(P〈0.05)。两组患者经治疗后,NIHSS评分均较治疗前有所下降,同组治疗前后差异有统计学意义(P〈0.05、0.01);治疗5、10 d,治疗结束时治疗组NIHSS评分均显著低于同一时间点对照组的评分,两组差异有统计学意义(P〈0.05、0.01)。从治疗10 d开始,两组患者白细胞介素6(IL-6)、内皮素1(ET-1)、丙二醛(MDA)均较治疗前有所下降,白细胞介素13(IL-13)、超氧化物歧化酶(SOD)均较治疗前有所升高,同组治疗前后差异有统计学意义(P〈0.05、0.01)。治疗组IL-6和ET-1在治疗5、10 d,治疗结束后与对照组差异有统计学意义(P〈0.01);治疗组IL-13、SOD水平在治疗10 d、治疗结束时与对照组差异有统计学意义(P〈0.01);治疗组MDA水平在治疗结束后与对照组的差异有统计学意义(P〈0.01)。结论 依达拉奉能对急性脑梗死患者具有较好的疗效,其作用可能与清除自由基和抑制炎性氧化应激有关。
Objective To explore the clinical effect and mechanism of edaravone in the treatment of acute cerebral infarction. Methods Patients (121 cases) with acute cerebral infarction from March 2011 to March 2013 for the treatment in the First Affiliated Hospital of China Medical University were randomly divided into control (60 cases) and treatment (61 cases) groups. The patients in the control group accepted conventional treatment, and those in the treatment group treated with Edaravone Injection 30 mg add 0.9% sodium chloride solution 100 mL, iv infusion, 2 times/d, 10 d for one courses. NIHSS, proinflammatory /anti inflammatory cytokines, free radicals of before treatment, treatment for 5 and 10 d were compared after 1 -- 2 courses treatment. Results The efficacy on the patients in the treatment and control groups were 83.61% and 61.67%, and there was significant difference between the two groups (P 〈 0.05). After the treatment, the NIHSS scores in the two groups were decreased, and there was statistical significance before and after the treatment (P 〈 0.05,0.01); NIHSS score in the treatment group was significantly lower than that in the same time point in the control group for 5/10 d and at the end of the treatment (P 〈 0.05, 0.01). From the treatment of 10 d, interleukin 6 (IL-6), endothelin 1 (ET-1), and malondialdehyde (MDA) were decreased, while interleukin 13 (IL-13) and superoxide dismutase (SOD) were more increased than before the treatment in the two groups. The difference was statistically significant (P 〈 0.05, 0.01). The IL-6 and ET-1 of 5, 10 d and at the end of the treatment in treatment group were different compared with the control group, and the difference was statistically significant (P 〈 0.01). The IL-13 and the level of SOD in 10 d and at the end of the treatment in the treatment group were different compared with the control group (P 〈 0.01). At the end of the treatment, the level of MDA in the treatment and control groups was
出处
《现代药物与临床》
CAS
2014年第6期639-643,共5页
Drugs & Clinic