摘要
目的:探讨神经节苷脂+阿司匹林+阿托伐他汀三联疗法对脑梗死患者氧化应激及炎症反应的影响。方法:选择138例急性脑梗死患者,随机分为对照组、三联组各69例。对照组接受常规对症治疗联合阿司匹林、阿托伐他汀治疗,三联组接受常规对症治疗联合神经节苷脂、阿司匹林、阿托伐他汀三联疗法,均持续1月。对比两组患者治疗前后氧化应激、炎症反应的差异。结果:入院即刻,两组患者入院即刻血清中氧化应激指标、炎症介质含量的差异无统计学意义。治疗1周后、治疗4周后时,三联组血清中氧化应激指标ROS、AOPPs的含量较对照组低,SOD、CAT的含量较对照组高;血清中炎症介质IL-6、TNF-α、TGF-β的含量较对照组低,IL-4、IL-10、IL-13的含量较对照组高。结论:脑梗死患者接受神经节苷脂+阿司匹林+阿托伐他汀三联治疗,可有效抑制机体的全身氧化应激及炎症反应。
Objective:To investigate the effects of ganglioside + aspirin + atorvastatin triple therapy on oxidative stress and inflammatory response in patients with cerebral infarction.Methods:138 patients with acute cerebral infarction between July 2016 and July 2017 were divided into control group(n=69)and triple group(n=69)by random number table method.Control group accepted conventional symptomatic treatment combined with aspirin and atorvastatin therapy,triple group accepted conventional symptomatic treatment combined with ganglioside,aspirin and atorvastatin triple therapy,and both groups were treated for 1 month.The differences in oxidative stress and inflammatory response were compared between the two groups before and after treatment.Results:Immediately after admission,There was no statistically significant difference in serum levels of oxidative stress indexes and inflammatory mediators between the two groups.After 1 week of treatment and after 4 weeks of treatment,serum oxidative stress indexes ROS and AOPPs levels of triple group were lower than those of control group whereas SOD and CAT contents were higher than those of control group;serum inflammatory mediators IL-6,TNF-αand TGF-βlevels were lower than those of control group whereas IL-4,IL-10 and IL-13 levels were higher than those of control group.Conclusion:ganglioside + aspirin + atorvastatin triple therapy can effectively inhibit the systemic oxidative stress and inflammatory response in patients with cerebral infarction.
出处
《海南医学院学报》
CAS
2018年第1期117-120,共4页
Journal of Hainan Medical University
基金
四川省医学会课题项目(Q16025)~~
关键词
脑梗死
三联疗法
氧化应激
炎症反应
cerebral infarction
triple therapy
oxidative stress
inflammatory response
