Dexmedetomidine reduces the apoptosis of rat hippocampal neurons via mediating ERK1/2 signal pathway by targeting miR-155

被引:6
|
作者
Zhu, Yun-Sheng [1 ]
Liu, Zhen [1 ]
Min, Jia [1 ]
Xiong, Ying-Fen [1 ]
机构
[1] Nanchang Univ, Dept Anesthesiol, Affiliated Hosp 1, 17 Yongwaizheng St, Nanchang 330006, Jiangxi, Peoples R China
关键词
Dexmedetomidine; ERK1/2; Hippocampal cells; Apoptosis; OGD/R injury; CEREBRAL ISCHEMIA-REPERFUSION; OXIDATIVE STRESS; INDUCED INJURY; REGULATED KINASE; NEUROPROTECTION; ACTIVATION; EXPRESSION; PROTECTS; INFLAMMATION; INHIBITION;
D O I
10.1016/j.acthis.2021.151734
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Rat hippocampal neurons were isolated and divided into Normal, oxygen glucose deprivation/reoxygenation (OGD/R), OGD/R + DEX, OGD/R + NC mimic, OGD/R + miR-155 mimic and OGD/R + DEX + miR-155 mimic groups. In OGD/R group, LDH, ROS and MDA levels and apoptosis rate was increased, with up-regulations of miR-155, Cyt c and Bax/Bcl-2 ratio, but decreases of SOD, GSH-Px and MMP levels, as well as down-regulations of p-ERK1/2/ERK1/2. As compared to the OGD/R group, parameters above in the OGD/R + DEX group were ameliorated evidently, while OGD/R + miR-155 mimic group manifested the opposite changes. Besides, miR-155 mimic could abolish the protective effect of DEX on the hippocampal neurons under OGD/R. DEX, via downregulating the expression of miR-155, could activate the ERK1/2 pathway, thereby mitigating the apoptosis and oxidative stress injury and increasing the MMP, thereby protecting hippocampal cells from OGD/R injury.
引用
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页数:6
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