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作 者:韩光[1,2] 李晓东[1,3] 唐健杰[1,4] 戴永逸[1] 王迪[1]
机构地区:[1]辽宁医学院基础医学院细胞生物学教研室,辽宁锦州121000 [2]辽宁省盘锦市中心医院,辽宁盘锦124000 [3]中国人民解放军第205医院重症医学科,辽宁锦州121000 [4]锦州市第二医院,辽宁锦州121000
出 处:《中国现代应用药学》2013年第7期715-718,共4页Chinese Journal of Modern Applied Pharmacy
基 金:锦州市科学技术计划项目(11A1E32);国家人力资源社会保障部留学人员科技活动项目(2011LX007)
摘 要:目的探讨辅酶Q10预处理对脑缺血再灌注损伤大鼠的保护作用及可能的相关机制。方法 90只成年SD大鼠,♂,随机分成假手术组(sham)、缺血再灌注组(I/R)、依达拉奉组(Y)、辅酶Q10预处理低剂量组(LQ)和高剂量组(HQ)。采用线栓法阻断大脑中动脉制备大鼠局灶性脑缺血再灌注模型,24 h后进行神经行为学评分,测定脑水含量;检测血清和脑组织中SOD活性及MDA含量;免疫组化检测Bcl-2、Bax和TNF-α表达情况。结果与I/R组相比,HQ组神经行为学评分明显降低,脑水含量显著减少,血清和脑组织中SOD活性升高,MDA含量降低。Bcl-2阳性表达率明显上升,Bax和TNF-α阳性表达率明显下降。结论辅酶Q10可能通过有效的减少自由基损伤,降低细胞凋亡和炎症因子水平对脑缺血再灌注损伤大鼠起到保护作用。OBJECTIVE To explore the protective effect of coenzyme Q10 on focal cerebral ischemic-reperfusion injured rats.METHODS Ninety adult male Sprague Dawley(SD) rats were randomly divided into 5 groups: sham-operated group(sham),ischemic-reperfusion group(I/R),Edaravone group(Y),coenzyme Q10 pre-treated low dose and high dose group(LQ and HQ).Models were established with middle cerebral artery occlusion.After 24 hours,neuroethology score and brain water content were detected.Activities of superoxide dismutase(SOD) and contents of malondialdehyde(MDA) were measured in blood serum and brain tissue from the experimental rats.The expression of Bcl-2,Bax and TNF-α protein were detected by immunohistochemistry staining.RESULTS Neuroethology score and brain water content significantly decreased in HQ group comparing with I/R group.Activities of SOD were higher and contents of MDA were lower in HQ group than I/R group in both blood serum and brain tissue.Immunohistochemistry staining showed that the positive cell number of expressing Bcl-2 significantly increased and the positive cell number of expressing Bax and TNF-α significantly decreased in HQ group compared with I/R group.CONCLUSION Coenzyme Q10 may protect rats from ischemic-reperfusion injury through scavenging free radicals and improving the anti-oxidative ability of the brain tissue and decreasing cell apoptosis and the level of inflammatory factors.
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