紫檀芪减轻小鼠缺血性脑损伤后神经细胞凋亡和氧化应激  

Pterostilbene can reduce the apoptosis and oxidative stress of neural cells after ischemia reperfusion injury in mice

作　　者：田士来 康军林 魏玉娥 武志 郑茂华[1] 火雷鸣[1] Tian Shilai;Kang Junlin;Wei Yu’e;Wu Zhi;Zheng Maohua;Huo Leiming(Department of Neurosurgery,The First Hospital of Lanzhou University,Lanzhou 730000,China;Department of Nursing Care,The First Hospital of Lanzhou University,Lanzhou 730000,China)

机构地区：[1]兰州大学第一医院神经外科,兰州730000 [2]兰州大学第一医院护理部,兰州730000

出　　处：《神经解剖学杂志》2022年第2期194-200,共7页Chinese Journal of Neuroanatomy

基　　金：甘肃省自然科学基金(20JR5RA354);兰州大学第一医院院内基金(ldyyyn2020-48)。

摘　　要：目的:探索紫檀芪(PTE)对小鼠缺血性脑损伤后凋亡及氧化应激的影响。方法:将雄性C57BL/6J小鼠分为4组,即假手术组(sham)、脑缺血再灌注损伤组(IR)、紫檀芪治疗组(PTE+IR)和ZnPP拮抗紫檀芪治疗组(PTE+ZnPP+IR),其中PTE的剂量为5 mg/kg,于建立模型(IR)前连续5 d每天腹腔给药1次,ZnPP以3 mg/kg的剂量于IR前30 min及IR后24 h分别腹腔给药1次;然后于缺血性脑损伤后48 h进行脑钠离子(Na^(+))含量测定;于缺血性脑损伤后6、24及48 h(IR6、IR24及IR48 h)使用TUNEL试剂盒检测细胞凋亡,Western Blot检测Bcl-2、Bax及HO-1蛋白的表达,OxyBlot蛋白氧化试剂盒检测羰基含量。结果:PTE可降低脑缺血再灌注损伤后小鼠缺血侧脑组织Na+含量、抑制脑细胞凋亡、降低Bax/Bcl-2的比值和上调HO-1的表达,同时PTE可减轻小鼠缺血侧脑组织的氧化应激反应,但是PTE的这些神经保护作用可被ZnPP逆转。结论:PTE在小鼠脑缺血再灌注损伤中具有明确的神经保护作用,其机制与抗氧化应激及抑制细胞凋亡有关。Objective:To explore the effects of pterostilbene(PTE)on apoptosis and oxidative stress after ischemia-reperfusion(IR)injury in mice.Methods:The C57BL/6J male mice were randomly divided into four groups:sham group,IR group,PTE+IR group,PTE+IR+ZnPP group.The dose of PTE used was 5 mg/kg once a day for 5 days totally before IR,and the dose of zinc protoporphyrin(ZnPP)used was 3 mg/kg at 30 minutes before IR and 24 h after IR by intraperitoneal injection.The brain sodium content was assessed at 48 h for contralateral and ipsilateral cerebrum by dried weight after IR.The apoptotic ratio in IR-injured brain were detected by TdT-mediated dUTP nick end labeling(TUNEL)and the protein expression of Bcl-2 and Bax were detected by Western Blot.The oxidative stress in IR-injured brain was detected by the protein expression of HO-1 by Western Blot and the protein carbonyl content by OxyBlot^(TM) protein oxidation detection kit.Results:PTE lowered brain sodium content,inhibited neuronal apoptosis,decreased the ratio of Bax/Bcl-2 and up-regulated the expression of HO-1,and reduced oxidative stress reaction of ipsilateral cerebral hemisphere after ischemia-reperfusion(IR)injury in mice.However,the neuroprotective effect of PTE was reversed by ZnPP.Conclusion:PTE paly a neuroprotective role against ischemia reperfusion in mice by suppression of cell apoptosis and oxidative stress reaction.

关 键 词：紫檀芪 脑缺血再灌注损伤 凋亡 氧化应激 小鼠 

分 类 号：R285.5[医药卫生—中药学]