丹参酮ⅡA对大鼠脑缺血再灌注后细胞凋亡、Drp-1、TRPM7表达的影响  

The effect of tanshinone ⅡA on apoptosis and the expression of, Drp-1 and TRPM7 in a rat model of cerebral ischemia reperfusion.

作　　者：肖晗 汤其强 刘磊磊 韩若东 

机构地区：[1]安徽医科大学附属省立医院神经内科 ,合肥230000 [2] 亳州市人民医院重症监护室

出　　处：《中国神经精神疾病杂志》2013年第12期719-723,共5页Chinese Journal of Nervous and Mental Diseases

基　　金：安徽省卫生厅医学科研课题(编号:2010B003)

摘　　要：目的探讨丹参酮ⅡA对大鼠局灶性脑缺血再灌注后细胞凋亡、Drp-1、TRPM7表达的影响。方法分别用高低剂量丹参酮ⅡA预处理大鼠,制备局灶性脑缺血模型,缺血2 h后开始监测缺血区大脑中动脉脑血流变化直到再灌注24 h,2,3,5-氯化三苯基四氮唑(2,3,5-triphenyltetrazolium chloride,TTC)染色法检测脑梗死体积,原位末端标记(in situ nick-end labeling,TUNEL)检测神经元凋亡,免疫组化及Western blot检测发动相关蛋白-1(dynamin-related protein 1,Drp-1)、瞬时受体电位离子通道蛋白7(transient Receptor Potential cation channel7,TRPM7)蛋白表达水平。结果丹参酮ⅡA高低剂量组能明显抑制缺血区脑组织Drp-1及TRPM7蛋白表达(P<0.05),减少凋亡细胞数(P<0.05),缩小脑梗死体积(P<0.05)。缺血2 h后再灌注24 h,I/R组右侧大脑中动脉缺血区血流量下降为31.80%±2.49%,与I/R组比较,I/R+Tan1组及I/R+Tan2组血流量分别为(54.8%±3.27%)、(58.8%±3.03%),P<0.05,但丹参酮ⅡA高低剂量组两者之间的脑梗死体积、TUNEL阳性细胞数、对脑血流量的改善无差异性(P>0.05)。结论丹参酮ⅡA对大鼠局灶性脑缺血再灌注后神经元凋亡及线粒体裂解有抑制作用,其机制可能与改善缺血区脑血流量,减少Drp-1、TRPM7表达有关。Objective To explore the effect of Tanshinone IIA on apoptosis and expression of Drp-1 and TRPM7 in a rat model of focal cerebral ischemia and reperfusion. Methods Rats were pretreated with high or low dose of tanshinone IIA before 2 h-focal cerebral ischemia plus 24 h-reperfusion. Cerebral blood flow in the middle cerebral artery was moni-tored during reperfusion. TTC, TUNEL and western blotting were used to detect the volume of cerebral infarction, apopto-sis and the protein expression of Drp-1 as well as TRPM7, respectively. Results Compared with control group, pretreat-ment with Tanshinone IIA could significantly down-regulate the expression of protein Drp-1 and TRPM7 （P〈0.05）, attenu-ate apoptosis （P〈0.05）, and reduce the volume of ischemia infarction. The volumes of right middle cerebral artery blood flow were（31.80%± 2.49%）,（54.8%± 3.27%）, and（58.8%± 3.03%）in controls, low-dose and high dose of tanshinone, respectively. Both low-dose and high-dose tanshinones improved cerebral blood flow. （tanshinone vs. control;all P〈0.05）. However, there was no statistical difference between low-dose and high-dose Tanshinone IIA groups in all measured out-comes （P〉0.05）. Conclusions Tanshinone IIA can inhibit ischemia-induced neuronal apoptosis and mitochondrial fission＆amp;nbsp;probably through improving cerebral artery blood flow and reducing the overexpression of Drp-1,TRPM7.

关 键 词：丹参酮IIA 再灌注 脑 细胞凋亡 

分 类 号：R743.3[医药卫生—神经病学与精神病学]