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Article Abstract
The present study aimed to investigate the function of micro (mi)RNA‑153 against isoflurane‑induced neurotoxicity and its mechanism. In isoflurane‑induced mice, miRNA‑153 expression was downregulated compared with in the control group. Downregulation of miRNA‑153 induced neurocyte apoptosis, reduced cell growth and promoted oxidative stress in an in vitro model. Overexpression of miRNA‑153 reduced oxidative stress, promoted cell growth and inhibited neurocyte apoptosis within an in vitro model. Downregulation of miRNA‑153 suppressed nuclear erythroid‑2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway, which was induced via the overexpression of miRNA‑153 in vitro. The Nrf2 agonist, dimethyl fumarate (2.5 µM), induced the Nrf2/ARE signaling pathway and reduced oxidative stress to induce neurocyte apoptosis in vitro following treatment with anti‑miRNA‑153. The results of the present study suggested the function of miRNA‑153 against neurotoxicity via Nrf2/ARE‑mediated cytoprotection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6471563 | PMC |
| http://dx.doi.org/10.3892/mmr.2019.10056 | DOI Listing |
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