羟基红花黄色素A与芍药苷联用对脑缺血再灌注大鼠脑组织p-AKT蛋白的影响  

Effect of HSYA and Paeoniflorin Combination on Expression of p-AKT in Rats with Cerebral Ischemia-reperfusion Injury

作　　者：余梦黎 秦莎莎[2] 廖金明 徐愉林 郑丽娴 朱原 姚晖 张继平 YU Mengli;QIN Shasha;LIAO Jinming;XU Yulin;ZHENG Lixian;ZHU Yuan;YAO Hui;ZHANG Jiping(Guangdong Medical University,Zhanjiang 524023 Guangdong,China;Guangdong Pharmaceutical University,Guangzhou 510006 Guangdong,China;Affiliated Foshan Hospital of Southern Medical University,Foshan 528000 Guangdong,China)

机构地区：[1]广东医科大学,广东湛江524023 [2]广东药科大学,广东广州510006 [3]南方医科大学附属佛山医院,广东佛山528000

出　　处：《中药新药与临床药理》2018年第1期13-18,共6页Traditional Chinese Drug Research and Clinical Pharmacology

基　　金：广东省中医药局2015年建设中医药强省科研课题(20152074);佛山市科技攻关项目(2016AB002981);佛山市"十三五"医学重点专科建设项目(FSZDZK135025)

摘　　要：目的探讨羟基红花黄色素A(HSYA)与芍药苷(PF)联用对脑缺血再灌注大鼠脑组织磷酸化蛋白激酶B(p-AKT)的影响。方法将160只SD大鼠随机分成HSYA组(5 mg·kg^(-1))、PF组(5 mg·kg^(-1))、预防治疗组(HSYA+PF,各5 mg·kg^(-1))、治疗组(HSYA+PF,各5 mg·kg^(-1))、银杏内酯组(5 mg·kg^(-1))、模型组、假手术治疗组(HSYA+PF,各5 mg·kg^(-1))、假手术空白组。采用右侧大脑中动脉线栓法(MACO)复制急性局灶性脑缺血再灌注模型,预防治疗组从造模前3 d开始通过尾静脉注射给药,余各组造模后连续给药7 d。再灌注6 h后及取材前进行神经行为评分;氯化三苯基四氮唑(TTC)染色观察并测定脑梗死面积百分比;HE染色观察各组大鼠海马区病理组织学变化;免疫组化法检测脑组织皮层区p-AKT蛋白表达情况。结果与假手术组比较,其余各组首次神经行为评分均显著增加(P<0.05);与模型组比较,预防治疗组首次神经行为评分显著降低(P<0.05),各给药组治疗后神经行为评分显著降低(P<0.05)。与假手术组比较,模型组脑梗死面积百分比显著增大(P<0.05);与模型组比较,各给药组脑梗死面积百分比显著减小(P<0.05)。与模型组比较,预防治疗组、治疗组、银杏内酯组的脑组织皮层内p-AKT阳性细胞表达率显著升高(P<0.05),而HSYA组、PF组与模型组的差异无统计学意义(P>0.05);与治疗组比较,预防治疗组的p-AKT阳性细胞表达明显增加(P<0.05)。结论 HSYA与PF联用较单用对脑缺血再灌注损伤有更强的保护作用,这可能与其上调PI3K/AKT通路中p-AKT蛋白的表达量有关,且预防用药的保护作用更强。Objective To explore the effect of hydroxyl safflower yellow A(HSYA) and paeoniflorin(PF) combination on expression of p-AKT in rats with cerebral ischemia reperfusion(I/R) injury.Methods One hundred and sixty Sprague-Dawley(SD)rats were randomly divided into HSYA group(5 mg·kg^-1),PF group(5 mg·kg^-1),preventive treatment group(HSYA and PF,5 mg·kg^-1 each),treatment group(HSYA and PF,5 mg·kg^-1 each),Ginkgo lactone group(5 mg·kg^-1),model group,control treatment group(HSYA and PF,5 mg·kg^-1 each),blank control group.The transient focal cerebral I/R model was established by a right middle cerebral artery occlusion(MCAO).Preventive treatment group was administrated drugs via tail-vein injection 3 days before the rats model was established,and the rest of the groups were provided the correspondent treatment immediately after modeling for 7 days.Neurological deficit symptom scores were evaluated after reperfusion 6 hours and before drawing materials.Infarct size was measured by 2,3,5-Triphenyltetrazolium Chloride(TTC) staining,morphological changes in hippocampal CA1 region were observed by hematoxylin eosin(HE) staining.The expression of p-AKT protein in cerebral cortex of rats was examined by immunohistochemistry(IHC).Result In contrast to the control group,the first neurological deficit symptom scores in the rest of the groups increased significantly.In contrast to the model group,the first neurological deficit symptom scores in the preventive treatment group decreased significantly(P < 0.05);the neurological deficit symptom scores in each treatment group decreased significantly after treatments(P < 0.05);the infarct area in model group rats was significantly larger than that in the blank control group.The infarct area in various treatment groups were significantly smaller than that in model group(P < 0.05);compared with the model group,the positive expression of p-AKT protein in preventive treatment group,treatment group and Ginkgo lactone group increased obviously(P <0.05),while the difference between HSY

关 键 词：羟基红花黄色素A 芍药苷 脑缺血再灌注 磷酸化蛋白激酶B 

分 类 号：R285.5[医药卫生—中药学]