Abstract
This study focused on exploring the neuroprotective role of Dexmedetomidine (DEX) and miR-206 in H2O2-induced SK-N-SH cells. First, we dectected the cell viability, apotosis, oxidative stress and miR-206 expression in H2O2-treated SK-N-SH cells.Next, we examined above content in H2O2-induced SK-N-SH cells though DEX treatment. Besides, the level of cell viability, apotosis, oxidative stress were evaluated in H2O2-treated SK-N-SH cells transfected with miR-206 mimics and miR-206 inhibitor. Moreover, the target gene of miR-206 were predicted and verifed by binformatics tools and luciferase reporter assay. These data indicated that H2O2 evoked the apotosis, oxidative stress and inhibition of miR-206 expression in SK-N-SH cells in a dose manner. Besides, DEX attenuated H2O2-induced oxidative damage, apotosis and promoted miR-206 expression in SK-N-SH cells. Moreover, overexpression of miR-206 augmented the cell viablity as well as suppressed apotosis and oxidative stress in H2O2-induced SK-N-SH cells, while down-expression of miR-206 showed opppsite effects. Further, Annexin A1 (ANXA1) was verified as a directly target of miR-206, and over-expression of ANXA1 could slack the neuroprotective effect of miR-206 in H2O2-induced SK-N-SH cells. DEX exerted neuroprotective effects on H2O2-treated SK-N-SH cells in vitro by negatively reguating ANXA1 expression via activation of miR-206.
Highlights
It is widely recognized that, hypoxic–ischaemic brain damage (HIBD) is a fatal neurological injury in newborn infants and the patients with stroke or cardiac arrest, which has become a major public health issues worldwide in past decades, leading to a high alarming cognitive impairment and mortality (Disdier & Stonestreet, 2020)
In recent years, increasing studies indicated that DEX can provide neuroprotective effects against HIBD in multiple ways, such as inhibition of apoptosis, blocking the release of inflammatory cytokines and relieving oxidative stress, which is able to improve the cognitive function under the condition of hypoxia-ischemia (Degos et al, 2013; Ren et al, 2016; Akpınar et al, 2016)
We found that DEX was able to significantly enhance cell viability, reduce apoptosis, lower cellular MDA, Lactate Dehydrogenase (LDH) and Reactive Oxygen Species (ROS) levels in H2O2 –treated SK-N-SH cells, which acted a protective role in neurocytes the after oxidative stress injury
Summary
It is widely recognized that, hypoxic–ischaemic brain damage (HIBD) is a fatal neurological injury in newborn infants and the patients with stroke or cardiac arrest, which has become a major public health issues worldwide in past decades, leading to a high alarming cognitive impairment and mortality (Disdier & Stonestreet, 2020). In recent years, increasing studies indicated that DEX can provide neuroprotective effects against HIBD in multiple ways, such as inhibition of apoptosis, blocking the release of inflammatory cytokines and relieving oxidative stress, which is able to improve the cognitive function under the condition of hypoxia-ischemia (Degos et al, 2013; Ren et al, 2016; Akpınar et al, 2016). With the deepening of researches, some studies have shown that miR-206 is closely involved in regulating ischemia-reperfusion injury (Kong et al, 2019), oxidative stress damage (Ciesla et al, 2016) and neuroprotection (Zhao et al, 2019). We focused on the molecular mechanism of H2O2-induced cytotoxicity, apoptosis and oxidative stress damage, and the associated roles of DEX and miR-206 of neuroprotective effect on SK-N-SH cells. We identified that DEX protected SK-N-SH cells from cytotoxicity, apoptosis and oxidative damage through regulation of miR-199a and subsequent down-regulated ANXA1 expression
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