缺血预处理减轻兔股动脉穿刺所致的血管内皮损伤

doi:10.16352/j.issn.1001-6325.2022.12.1817

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.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 Miao^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/Abstract

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

中图分类号:

R543.2

刘鹏, 李凯园, 杨阳, 满艺龙, 杜凤立, 刘淼. 缺血预处理减轻兔股动脉穿刺所致的血管内皮损伤[J]. 基础医学与临床, 2022, 42(12): 1817-1822.

LIU Peng, LI Kai-yuan, YANG Yang, MAN Yi-long, DU Feng-li, LIU Miao. Ischemic preconditioning attenuates endothelial injury induced by femoral artery puncture in rabbits[J]. Basic & Clinical Medicine, 2022, 42(12): 1817-1822.

参考文献 13

[1]	Chen Y, Ke Z, Xiao J, et al. Subcutaneous injection of nitroglycerin at the radial artery puncture site reduces the risk of early radial artery occlusion after transradial coronary catheterization: a randomized, placebo-controlled clinical trial[J]. Circ Cardiovasc Interv, 2018, 11, doi: 10.1161/CIRCINTERVENTIONS.118.006571.
[2]	Chen C, Sun L, Zhang W, et al. Limb ischemic preconditioning ameliorates renal microcirculation through activation of PI3K/Akt/eNOS signaling pathway after acute kidney injury[J]. Eur J Med Res, 2020, 25: 10.doi:10.1186/s40001-020-00407-4.
[3]	Torregroza C, Glashoerster CO, Feige K, et al. Mediation of the cardioprotective effects of mannitol discovered, with refutation of common protein kinases[J]. Int J Mol Sci, 2021, 22, doi: 10.3390/ijms222212471.
[4]	Saxena R, Weintraub NL, Tang Y. Optimizing cardiac ischemic preconditioning and postconditioning via epitranscriptional regulation[J]. Med Hypotheses, 2020, 135:109451. doi: 10.1016/j.mehy.2019.109451.
[5]	李贞燕, 陈敏, 戴日蕾,等. PI3K和Akt在心血管疾病中的作用[J]. 基础医学与临床, 2019, 39: 1200-1204.
[6]	Stiles BL. PI-3-K and AKT: Onto the mitochondria[J]. Adv Drug Deliv Rev, 2009, 61: 1276-1282.
[7]	Arab HH, Salama SA, Maghrabi IA. Camel milk attenuates methotrexate-induced kidney injury via activa-tion of PI3K/Akt/eNOS signaling and intervention with oxidative aberrations[J]. Food Funct, 2018, 9: 2661-2672.
[8]	Liu M, Kong Q, Cai X, et al. Influence of remote ischemic conditioning on radial artery occlusion[J]. Heart Vessels, 2019, 34: 771-776.
[9]	Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium[J]. Circulation, 1986, 74: 1124-1136.
[10]	Bang JY, Kim SG, Oh J, et al. Impact of remote ischemic preconditioning conducted in living kidney donors on renal function in donors and recipients following living donor kidney transplantation: a randomized clinical trial[J]. J Clin Med, 2019, 8, doi: 10.3390/jcm8050713.
[11]	Sung HY, Choi EN, Han J, et al. Protective role of ABCA1 in ischemic preconditioning is mediated by downregulation of miR-33-5p and miR-135-5p[J]. Sci Rep, 2021, 11: 12511.doi:10.1038/s41598-021-91982-x.
[12]	Duan MX, Zhou H. Andrographolide protects against HG-induced inflammation, apoptosis, migration, and impairment of angiogenesis via PI3K/AKT-eNOS signaling in HUVECs[J]. Mediators Inflamm, 2019, 2019: 6168340. doi: 10.1155/2019/6168340.eCollection 2019.
[13]	Xu Y, Sui L, Qiu B, et al. ANXA4 promotes trophoblast invasion via the PI3K/Akt/eNOS pathway in preeclampsia[J]. Am J Physiol Cell Physiol, 2019, 316: C481-C491.

[1]	徐云聪, 郑金旭. CD27/CD70与特发性肺纤维化[J]. 基础医学与临床, 2024, 44(8): 1170-1174.
[2]	姚安军, 陈凌子, 金惠仙. 二十二碳六烯酸抑制人结肠癌细胞系HT-29增殖[J]. 基础医学与临床, 2024, 44(8): 1107-1112.
[3]	潘闪, 林铿强, 陈树兴. 培美曲塞抑制人肺腺癌细胞系A549增殖[J]. 基础医学与临床, 2023, 43(9): 1359-1363.
[4]	刘湛傲, 陈晨. 卵泡体外激活在早发性卵巢功能不全患者辅助生殖中的研究进展[J]. 基础医学与临床, 2023, 43(4): 538-546.
[5]	刘珈言, 梅蓉, 杨礼凤, 赵文彬, 韩成龙, 周慧, 李二龙. 雷公藤多苷减轻干燥综合征模型小鼠炎性反应[J]. 基础医学与临床, 2022, 42(9): 1362-1366.
[6]	杨芒庄, 杨旭东, 王晓龙. Circ-MALAT1靶向miR-101抑制膀胱癌细胞系SW780侵袭和迁移[J]. 基础医学与临床, 2022, 42(3): 472-478.
[7]	秦建民, 张来香, 魏振英. miR-193a-3p抑制高糖诱导人视网膜血管内皮细胞凋亡[J]. 基础医学与临床, 2021, 41(7): 995-1000.
[8]	徐林飞, 张海涛, 刘晟, 蔡海荣, 胡恩平. 白花蛇舌草上调miR-485-5p抑制人膀胱癌细胞系KU-19-19增殖、迁移和侵袭[J]. 基础医学与临床, 2021, 41(6): 842-847.
[9]	吴晨瑞, 何虹兵, 程予琦, 毛岚田, 廖正步. 重组人促红细胞生成素改善小鼠创伤性脑损伤神经功能[J]. 基础医学与临床, 2020, 40(3): 289-293.
[10]	王炀佳, 张佳, 李宾, 曾翔俊. Apelin-13通过eNOS/NO促进糖尿病小鼠主动脉细胞焦亡相关蛋白的表达[J]. 基础医学与临床, 2020, 40(2): 155-160.
[11]	郭亚东吴红娟孙要文. PODXL参与瘢痕疙瘩成纤维细胞的过度增殖[J]. 基础医学与临床, 2019, 39(9): 1243-1247.
[12]	吴艳张铭鲁开智陈杨. 腺苷A2b受体激活减轻小鼠肾缺血再灌注致肺损伤[J]. 基础医学与临床, 2019, 39(8): 1102-1107.
[13]	轩辕东刘雅娟任永康徐璐朱娜杨锐英. 脂联素抑制高浓度胰岛素诱导的大鼠心肌细胞肥大[J]. 基础医学与临床, 2018, 38(8): 1064-1068.
[14]	沈冰冰张松朱启仁王志荣张卓琦. 羟基红花黄色素A减轻大鼠心肌细胞缺氧/复氧损伤[J]. 基础医学与临床, 2018, 38(4): 480-484.
[15]	石红冯江敏. 丹参酮ⅡA抑制马兜铃酸诱导HUVECs凋亡及其可能机制[J]. 基础医学与临床, 2016, 36(9): 1216-1221.

缺血预处理减轻兔股动脉穿刺所致的血管内皮损伤

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

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 13

相关文章 15

编辑推荐

Metrics

本文评价