基础医学与临床 ›› 2022, Vol. 42 ›› Issue (12): 1817-1822.doi: 10.16352/j.issn.1001-6325.2022.12.1817

• 研究论文 •    下一篇

缺血预处理减轻兔股动脉穿刺所致的血管内皮损伤

刘鹏1, 李凯园1, 杨阳1, 满艺龙1, 杜凤立2, 刘淼1*   

  1. 1.山东第一医科大学附属中心医院 心血管内科,山东 济南 250000;
    2.山东省公共卫生临床中心,山东 济南 250000
  • 收稿日期:2021-12-06 修回日期:2022-05-06 出版日期:2022-12-05 发布日期:2022-11-23
  • 通讯作者: * 836518522@qq.com
  • 基金资助:
    国家科技重大专项课题(2020ZX09201025)

Ischemic preconditioning attenuates endothelial injury induced by femoral artery puncture in rabbits

LIU Peng1, LI Kai-yuan1, YANG Yang1, MAN Yi-long1, DU Feng-li2, LIU Miao1*   

  1. 1. Department of Cardiovascular Medicine, Affiliated Central Hospital of Shandong First Medical University, Jinan 250000;
    2. Shandong Clinical Center of Public Health, Jinan 250000, China
  • Received:2021-12-06 Revised:2022-05-06 Online:2022-12-05 Published:2022-11-23
  • Contact: * 836518522@qq.com

摘要: 目的 探讨缺血预处理(IP)是否减轻兔动脉穿刺引起的内皮损伤。方法 将兔分为对照组、缺血预处理组(IP组)、股动脉穿刺组(P组)和缺血预处理+股动脉穿刺组(IP-P组)。用免疫组化测定血管内皮组织磷酸肌醇-3-激酶(PI3K)、蛋白激酶B(AKT)和一氧化氮合成酶(eNOS)的相对表达量,蛋白印迹法(Western blot)检测p-AKT和p-eNOS的表达,RT-qPCR检测eNOS mRNA相对表达量,酶联免疫吸附法(ELISA)检测血浆一氧化氮(NO)含量。结果 IP-P组血管内皮中PI3K、AKT和eNOS的相对表达量高于P组,低于IP组(P<0.05)。IP-P组p-AKT和p-eNOS的相对表达量高于P组(P<0.05)。IP-P组eNOS的相对表达量高于P组,低于IP组(P<0.05)。IP-P组血浆NO含量高于P组,低于IP组(P<0.05)。结论 IP可以促进兔血管内皮eNOS磷酸化和NO合成,这可能是动脉穿刺前IP减少内皮损伤的机制之一。

关键词: 缺血预处理, 股动脉穿刺, PI3K/AKT, eNOS

Abstract: Objective To investigate whether ischemic preconditioning (IP) attenuates endothelial injury induced by arterial puncture. Methods Rabbits were divided into control group, ischemic preconditioning group (IP group), femoral artery puncture group (P group) and ischemic preconditioning+femoral artery puncture group (IP-P group). The expression of PI3K, AKT and eNOS in endothelial tissue was determined by immuno-histochemistry. p-AKT and p-eNOS were detected by Western blot. eNOS was detected by RT-qPCR. Plasma NO was detected by enzyme-linked immunosorbent assay(ELISA). Results The expression of PI3K, AKT and eNOS in the vascular endothelium of IP-P group was higher than that from P group and lower than that from IP group(P<0.05). The expression of p-AKT and p-eNOS in IP-P group was higher than that from P group(P<0.05). The expression of eNOS in IP-P group was higher than that from P group and lower than that from IP group(P<0.05). Plasma NO level in IP-P group was higher than that in P group and lower than that in IP group (P<0.05). Conclusions IP promotes eNOS phos-phorylation and NO synthesis in rabbit vascular endothelium, which may be one of the potential mechanisms by which IP reduces endothelial injury before arterial puncture.

Key words: ischemic preconditioning, femoral artery puncture, PI3K/AKT, eNOS

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