丹参酮ⅡA对早期脑缺血和脑缺血再灌注损伤的脑保护作用  

Neuroprotective effect of Tanshinone ⅡA on early cerebral ischemia and cerebral ischemia-reperfusion models

作　　者：韩若东 汤其强[1] 肖晗[1] 李俊[2] 

机构地区：[1]安徽医科大学附属省立医院神经内科,合肥230001 [2]安徽医科大学药学院,合肥230032

出　　处：《安徽医科大学学报》2012年第6期655-658,共4页Acta Universitatis Medicinalis Anhui

基　　金：安徽省自然科学基金(编号:090413120);安徽省卫生厅医学科研课题(编号:2010B003);安徽省高校自然科学研究项目(编号:KJ2007B147)

摘　　要：目的观察丹参酮ⅡA对大鼠早期脑缺血和脑缺血再灌注模型的脑保护作用及可能机制。方法 SD大鼠随机分为5组:假手术组、脑缺血2 h模型组、脑缺血2 h再灌注1h模型组、脑缺血2 h+丹参酮ⅡA组、脑缺血2 h再灌注1 h+丹参酮ⅡA组。丹参酮ⅡA以30 mg/kg灌胃,1次/d,假手术组、模型组用羧基纤维素钠代替。给药7 d后线栓法致大脑中动脉闭塞(MCAO)制备大鼠局灶性脑缺血再灌注模型。观察各组大鼠神经行为学评分(NBS),TUNEL法检测脑细胞凋亡,Western blot法检测脑梗死区Bax、Bcl-2的表达,TTC染色法检测脑梗死体积,试剂盒检测脑梗死区谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)含量。结果与模型组比较,丹参酮ⅡA能明显降低梗死侧脑组织的细胞凋亡、脑梗死体积及Bax的表达,并能提高NBS评分、增加GSH-Px的活性及Bcl-2的表达,但对MDA含量无明显影响。结论丹参酮ⅡA对大鼠早期脑缺血和脑缺血再灌注损伤具有脑保护作用,其机制可能是通过上调Bcl-2的表达、下调Bax的表达,增加GSH-Px的活性清除氧自由基,从而抑制细胞凋亡降低脑梗死体积,改善神经功能缺损评分。Objective To observe the neuroprotection of Tanshinone ⅡA and its possible mechanisms on rat early cerebral ischemia and ischemia-reperfusion. Methods SD rats were randomly divided into five groups ： sham group, ischemia for 2 h group, ischemia for 2 h/reperfusion for 1 h group, ischemia for 2 h ＋ Tanshinone ⅡA 30 mg/kg administered and ischemia for 2 h/reperfusion for 1 h ＋ Tanshinone ⅡA 30 mg/kg administered. Tanshinone ⅡA was gavaged once a day. Sham group and model group were garaged sodium carboxymethyl cellulose as a substitute. Af- ter administration for 7 days, suture method induced by middle cerebral artery occlusion （MCAO） to prepare focal cerebral ischemia and ischemia-reperfusion model. Neurobehavioral score （NBS） was evaluated in each group; TUNEL staining was used to measure apoptosis. Western blot was used to evaluate the protein expression of Bax and Bcl-2; The volume of cerebral infarction are evaluated by TTC staining; Glutathione peroxidase（GSH-Px） activities and contents of Malondialdehyde（MDA） of cerebral infarction were examined by kit. Results Compared with control group,Tanshinone ⅡA not only could decrease apoptosis, size of infarct volume and the expression of Bax of brain tissue in cerebral infarction area markedly, but also could improve the NBS ratings, increase glutathione peroxidase activities and the protein expression of Bcl-2. While there was no significant changes in MDA contents. Conclusion Tanshinone ⅡA has the neuroprotection on early cerebral ischemia and cerebral ischemia-reperfusion injury in rats. It may be related with up-regulating the expression of Bcl-2 and down-regulating the expression of Bax,increasing glutathione peroxidase activity, scavenging oxygen free radicals to inhibition of apoptosis, reducing infarct volume and improving neurological function.

关 键 词：丹参酮 脑缺血 再灌注损伤 BAX BCL-2 

分 类 号：R743.33[医药卫生—神经病学与精神病学] R285[医药卫生—临床医学]