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 down-regulating 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.

大鼠海马神经元被分离并分为正常，氧葡萄糖剥夺/复氧（OGD/R），OGD/R + DEX，OGD/R + NC模拟，OGD/R + miR-155模拟和OGD/R + DEX + miR -155 个模拟组。OGD/R组LDH、ROS和MDA水平升高，细胞凋亡率升高，miR-155、Cyt c和Bax/Bcl-2比值上调，SOD、GSH-Px和MMP水平降低，如以及 p-ERK1/2/ERK1/2 的下调。与OGD/R组相比，OGD/R+DEX组上述参数明显改善，而OGD/R+miR-155模拟组则呈现相反的变化。此外，miR-155模拟物可以消除OGD/R下DEX对海马神经元的保护作用。DEX 通过下调 miR-155 的表达，可以激活 ERK1/2 通路，