Minocycline induces protective autophagy in vascular endothelial cells exposed to an in vitro model of ischemia/reperfusion-induced injury

被引:21
作者
Dong, Wenbin [1 ]
Xiao, Shigeng [1 ]
Cheng, Min [1 ]
Ye, Xiaodi [1 ]
Zheng, Gaoli [1 ]
机构
[1] Zhejiang Acad Med Sci, Inst Mat Med, 182 Tianmushan Rd, Hangzhou 310013, Zhejiang, Peoples R China
关键词
minocycline; ischemia/reperfusion; autophagy; human umbilical vein endothelial cells;
D O I
10.3892/br.2015.554
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Minocycline has been reported to exhibit advantageous effects on ischemic stroke; however, the precise mechanism of minocycline remains to be established. In the present study, human umbilical vein endothelial cells (HUVECs) were subjected to in vitro simulated ischemia/reperfusion conditions to determine the potential effect of minocycline-induced autophagy on HUVEC damage under oxygen-glucose deprivation/reperfusion (OGD/R). The study demonstrated that minocycline enhanced autophagy in a dose-dependent manner in HUVECs exposed to OGD/R, and only low-dose minocycline protected HUVECs from OGD/R-induced damage. Subsequently, 3-methyladenine (3-MA) was added into the culture media and the protective effect of minocycline was abolished. At the same time, it has been observed that simultaneous treatment with 3-MA also inhibited the autophagy activity induced by minocycline. This finding could suggest that autophagy induced by minocycline serves as one of the potential protective mechanism underlying the beneficial effects of minocycline on ischemic injury.
引用
收藏
页码:173 / 177
页数:5
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