丹参酮ⅡA对脑缺血再灌注损伤大鼠的保护作用及其机制  

PROTECTION AND MECHANISM OF TANSHINONEⅡA ON ISCHEMICAL REPERFUSION INJURY RATS

作　　者：支文煜[1] 

机构地区：[1]江苏省常熟市第一人民医院药事部,213001

出　　处：《中国煤炭工业医学杂志》2010年第9期1365-1367,共3页Chinese Journal of Coal Industry Medicine

摘　　要：目的探讨丹参酮ⅡA(TanⅡA)对缺血再灌注损伤大鼠的保护作用及其抗凋亡机制。方法将SD大鼠随机分为假手术组、缺血再灌注组、TanⅡA低剂量治疗组、中剂量、高剂量治疗组,线栓法建立局灶性脑缺血再灌注模型。TanⅡA高、低剂量治疗组于术前连续灌胃给予高、低剂量TanⅡA7d,1次/d。WESTERN-BLOT观察缺血90min再灌注24h大鼠额顶部皮质Bcl-2和Bax蛋白表达,并进行2,3,5-三苯基氯化四氮唑(TTC)染色观察脑梗死体积。TUNEL染色观察凋亡细胞信号表达。处死前,进行神经行为学评分。结果脑缺血再灌注24h,缺血再灌注组Bax表达增加和Bcl-2表达减少,与假手术组比较,差异有统计学意义(P<0.05);与缺血再灌注组比较,TanⅡA高、低剂量治疗组均显著增加Bcl-2表达,减少Bax表达,高、低剂量组之间差异亦具有统计学意义(P<0.05)。TanⅡA高、低剂量治疗组脑梗死体积较缺血再灌注组减小,高、低剂量组之间差异具有统计学意义(P<0.05)。TanⅡA高、低剂量治疗组神经行为学评分明显高于缺血再灌注组,TanⅡA高剂量治疗组缺血改变亦好于低剂量治疗组。结论 TanⅡA对缺血再灌注脑损伤具有保护作用,其机制可能与增加Bcl-2蛋白表达同时降低Bax蛋白表达,从而产生抗凋亡作用有关。Objective To study the effect of tanshinone ⅡA（Tan ⅡA） on middle cerebral artery occlusion （MCAO） rats and its anti-apoptosis property. Methods Rats were randomly divided into 4 groups：sham operated group,I/R group,low dose Tan ⅡA treated group and high dose TanⅡA treated group. The focal MCAO model was made by suture-occluded method. Rats were pretreated with Tan ⅡA i.v for 7d,respectively. After 90 min MCAO following 24h of reperfusion,the expression of Bax and Bcl-2,and TUNAL staining of ischemic frontal and parietal cortex were investigated. TTC staining was used to calculate the cerebral infarct volume. Also,the neurological score was conducted. Results Compared with I/R group,cerebral infarction volume in low dose Tan ⅡA treated group and high dose Tan ⅡA treated group decreased in a dose-dependent manner （P〈0.05）. Compared with I/R group,low and high dose Tan ⅡA treated groups dose-dependently reduce the expression of Bcl-2 but increased the expression of Bax. The Tan ⅡA can also attenuate the apoptosis in cortex,which can be observed by TUNAL staining. Conclusion Tan ⅡA may alleviate cerebral ischemia-reperfusion injury by attenuating apoptosis.

关 键 词：脑缺血再灌注 凋亡相关蛋白 Bcl-2 CASPASE-3 丹参酮 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]