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. 2020 Aug 6;14:3177–3188. doi: 10.2147/DDDT.S262121

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© 2020 Yang et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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Effect of MT on miR-26a-5p and NRSF in CIRI in vitro and in vivo models. (A) miR-26a-5p is significantly downregulated in CIRI in vivo model, while MT can restore miR-26a-5p expression. (B–C) The expression of NRSF and protein level in CIRI in vivo model are significantly upregulated, while MT can silence NRSF and its protein map. (D) miR-26a-5p is significantly downregulated in the OGD/R in vitro model, and MT can upregulate the miR-26a-5p expression. (E–F) In vitro model of OGD/R, NRSF expression and protein level are significantly upregulated, MT can silence NRSF and its protein map.

Notes: Compared with sham or control, *represents P<0.05 and **represents P<0.01; compared with CIRI or OGD/R, ^#represents P<0.05.

Abbreviations: MT, melatonin; CIRI, cerebral ischemia-reperfusion injury; NRSF, neuron-restrictive silencing factor; miR, microRNA; OGD/R, oxygen-glucose deprivation/reperfusion; LC3, light chain 3; P62, sequestosome 1; TNF, tumor necrosis factor; IL, interleukin; MDA, malondialdehyde; GSHPx, glutathione peroxidase; SOD, superoxide dismutase.