右美托咪定预处理减轻氧糖剥夺再灌注条件下HUVECs的损伤

姚浩旗; 吴庆; 黄河; 李洪; 陈建; 杨天德

doi:10.16016/j.1000-5404.201711075

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右美托咪定预处理减轻氧糖剥夺再灌注条件下HUVECs的损伤

基础医学 | 更新时间：2026-01-09

- 右美托咪定预处理减轻氧糖剥夺再灌注条件下HUVECs的损伤
- Dexmedetomidine preconditioning ameliorates oxygen glucose deprivation and reperfusion injury in human umbilical vein endothelial cells
- 第三军医大学学报 2018年40卷第9期页码：801-804
- 作者机构：
  
  400037 重庆, 陆军军医大学(第三军医大学)第二附属医院麻醉科
- 作者简介：
  
  [杨天德, 电话:(023)68763638, E-mail:31011@sina.com YANG Tiande, Tel:86-23-68763638, E-mail:31011@sina.com
- 基金信息：
  
  第三军医大学新桥医院临床科研基金(2014D327)
- DOI：10.16016/j.1000-5404.201711075
  中图分类号： R322.123;R654.1;R971.3
- 收稿：2017-11-16，
  
  修回：2018-01-22，
  
  纸质出版：2018-05-15
- 稿件说明：
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姚浩旗, 吴庆, 黄河, 等. 右美托咪定预处理减轻氧糖剥夺再灌注条件下HUVECs的损伤[J]. 第三军医大学学报, 2018,40(9):801-804.

Haoqi YAO, Qing WU, He HUANG, et al. Dexmedetomidine preconditioning ameliorates oxygen glucose deprivation and reperfusion injury in human umbilical vein endothelial cells[J]. Journal of Third Military Medical University, 2018, 40(9): 801-804.
姚浩旗, 吴庆, 黄河, 等. 右美托咪定预处理减轻氧糖剥夺再灌注条件下HUVECs的损伤[J]. 第三军医大学学报, 2018,40(9):801-804. DOI： 10.16016/j.1000-5404.201711075.

Haoqi YAO, Qing WU, He HUANG, et al. Dexmedetomidine preconditioning ameliorates oxygen glucose deprivation and reperfusion injury in human umbilical vein endothelial cells[J]. Journal of Third Military Medical University, 2018, 40(9): 801-804. DOI： 10.16016/j.1000-5404.201711075.

摘要

目的

探讨右美托咪定预处理对氧糖剥夺再灌注条件下人脐静脉内皮细胞(human umbilical vein endothelial cell

HUVECs)的保护作用。

方法

体外培养HUVECs

分为4组:对照组(NC组)

ogd/r组(加入等体积的PBS)

Dex+ogd/r组(加入50 μmol/L的右美托咪定预处理2 h)

Dex+YOH+ogd/r组(加入50 μmol/L的右美托咪定和100 μmol/L育亨宾预处理2 h)。对照组置于正常条件下培养

其他3组细胞置于Hank’s液中于缺氧恒温细胞培养箱内培养12 h

之后换正常培养基置于常氧恒温培养箱内培养4 h。采用CCK-8试剂盒检测细胞活力

取细胞培养基上清液检测LDH活力。用流式细胞仪检测细胞内活性氧水平和钙离子水平

用Rhodamine-123检测细胞线粒体膜电位的高低。

结果

与NC组相比

ogd/r组细胞活力明显下降(

0.05)

LDH释放水平升高(

0.05)

胞内活性氧和钙离子水平升高(

0.05)

线粒体膜电位降低(

0.05);与ogd/r组相比

Dex+ogd/r组细胞活力升高(

0.05)

LDH释放水平降低(

0.05)

胞内活性氧和钙离子水平降低(

0.05)

线粒体膜电位升高(

0.05);与Dex+ogd/r组相比

Dex+YOH+ogd/r组细胞活力下降(

0.05)

LDH释放水平升高(

0.05)

胞内活性氧和钙离子水平升高(

0.05)

线粒体膜电位降低(

0.05)。

结论

右美托咪定预处理可以减轻氧糖剥夺再灌注造成的HUVECs损伤

可能与激活α受体有关。

Abstract

Objective

To investigate the effect of dexmedetomidine (Dex) preconditioning on oxygen glucose deprivation/reperfusion (ogd/r)-induced injury in human umbilical vein endothelial cells (HUVECs).

Methods

Cultured HUVECs were randomly divided into 4 groups (

=12)

that is

control group (NC)

ogd/r group (PBS)

Dex+ogd/r group (pretreatment of 50 μmol/L Dex for 2 h)

and Dex+Yohimbine (YOH) +ogd/r group (pretreatment of 50 μmol/L Dex and 100 μmol/L YOH for 2 h).The control group were cultured under normal condition

while the culture media of the other 3 groups were replaced with Hank's solution and the cells were placed in a hypoxia incubator for 12 h followed by normal condition for 4 h.CCK-8 assay was used to detect cell viability

and the activity of lactate dehydrogenase (LDH) in the supernatant was measured with LDH kit.Flow cytometry was adopted to detect the intracellular levels of reactive oxygen species (ROS) and calcium ion.Rhodamine-123 was employed to measure the trans-membrane potential of mitochondrion.

Results

Compared with the NC group

the cells in the ogd/r group had significantly decreased viability (

0.05)

increased LDH level (

0.05)

elevated intracellular ROS and calcium ion levels (

0.05)

and reduced trans-membrane potential of mitochondrion (

0.05).While

the cells in the Dex+ogd/r gro

up had significantly stronger cell viability (

0.05)

less secretion of LDH (

0.05)

decreased intracellular levels of ROS and calcium ion (

0.05)

and increased trans-membrane potential of mitochondrion (

0.05) when compared with the ogd/r group.In the Dex+YOH+ogd/r group

cell viability was decreased

LDH level was increased

the intracellular levels of ROS and calcium ion were elevated

but the trans-membrane potential of mitochondrion was significantly decreased when compared with the Dex+ogd/r group (all

0.05).

Conclusion

Dex preconditioning can effectively attenuate ogd/r-induced injury in HUVECs

which may be related to activation of alpha 2 adrenergic receptor.

关键词

Keywords

references

SINGHAL A K, SYMONS J D, BOUDINA S, et al .Role of endothelial cells in m yocardial ischemia-reperfusion injury[J ] .Vasc Dis Prev, 2010, 7:1-14.

CAI Y, XU H, YAN J, et al .Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury[J ] .Mol Med Reports, 2014, 9(5):1542-1550.DOI:10.3892/mmr.2014.2034.

HOFMANN U, FRANTZ S.Role of lymphocytes in myocardial injury, healing, and remodeling after myocardial infarction[J].Circulation Res, 2015, 116(2):354-367.DOI:10.1161/CIRCRESAHA.116.304072.

LIU J, WANG H, LI J.Inflammation and inflammatory cells in myocardial infarction and reperfusion injury:a double-edged sword[J].Clin Med Insights Cardiol, 2016, 10:79-84.DOI:10.4137/CMC.S33164.

LEMPIAINEN J, FINCKENBERG P, MERVAALA E E, et al . Dexmedetomidine preconditioning ameliorates kidney ischemia-reperfusion injury[J ] .Pharmacol Res Perspect, 2014, 2(3):e45.DOI:10.1002/prp2.45.

IBACACHE M, SANCHEZ G, PEDROZO Z, et al .Dexmedetomidine preconditioning activates pro-survival kinases and attenuates regional ischemia/reperfusion injury in rat heart[J ] .Biochim Biophys Acta, 2012, 1822(4):537-545.DOI:10.1016/j.bbadis.2011.12.0 13.

WANG Q, SHE Y, BI X, et al .Dexmedetomidine protects PC12 cells from lidocaine-induced cytotoxicity through downregulation of COL3A1 mediated by miR-let-7b[J ] .DNA Cell Biol, 2017, 36(7):518-528.DOI:10.1089/dna.2016.3623.

ZHANG F, DING T, YU L, et al .Dexmedetomidine protects against oxygen-glucose deprivation-induced injury through the I2 imidazoline receptor-PI3K/AKT pathway in rat C6 glioma cells[J ] .J Pharm Pharmacol, 2012, 64(1):120-127.DOI:10.1111/j.2042-7158.2011.01382.x.

ZWEIER J, TALUKDER M.The role of oxidants and free radicals in reperfusion injury[J].Cardiovasc Res, 2006, 70(2):181-190.DOI:10.1016/j.cardiores.2006.02.025.

DAVIDSON S M, DUCHEN M R.Endothelial mitochondria:contributing to vascular function and disease[J].Circ Res, 2007, 100(8):1128-1141.DOI:10.1161/01.RES.0000261970.18328.1d.

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