Abstract
BackgroundPropofol is an intravenous anesthetic agent that commonly induces significant neuroapoptosis. MicroRNAs (miRNAs) have been reported to participate in the regulation of propofol exposure-mediated neurotoxicity. MiR-215, as one of miRNAs, was found to regulate nerve cell survival. However, the mechanism through which miRNAs regulate propofol exposure-mediated neurotoxicity is still unclear.MethodsReal-time PCR was used to detect miR-215 expression level. Cell viability was measured using MTT assay. Cell apoptosis was examined via flow cytometry analysis. ROS, MDA, LDH and SOD levels were assayed through ELISA kits. Dual luciferase reporter assay identified the interaction between miR-215 and large tumor suppressor 2 (LATS2). Protein level was detected using western blot analysis.ResultsMiR-215 expression was downregulated in propofol-treated rat hippocampal neurons. MiR-215 mimics promoted cell viability and reduced apoptosis in propofol-treated neonatal rat hippocampal neuron. MiR-215 mimics also caused inhibition of oxidative stress as evidenced by suppression of ROS, MDA and LDH levels as well as increase of SOD level. In addition, we found that large tumor suppressor 2 (LATS2) is a target of miR-215 and miR-215 mimics decreased LATS2 level in propofol-treated neonatal rat hippocampal neuron. Further, LATS2 overexpression suppressed the effect of miR-215 on propofol-induced apoptosis and oxidative stress in neonatal rat hippocampal neuron.ConclusionTaken together, we demonstrate that miR-215 attenuates propofol-induced apoptosis and oxidative stress in neonatal rat hippocampal neuron by targeting LATS2, suggesting that miR-215 may provide a new candidate for the treatment of propofol exposure-induced neurotoxicity.
Highlights
Propofol is an intravenous anesthetic agent that commonly induces significant neuroapoptosis
These results indicate that miR-215 has a suppressive role in propofol-induced apoptosis in neonatal rat hippocampal neuron
Downregulation of large tumor suppressor 2 (LATS2) induced by miR-215 overexpression in propofol-treated neonatal rat hippocampal neuron We examined the effect of miR-215 overexpression on LATS2 in propofol-treated neonatal rat hippocampal neuron
Summary
Propofol is an intravenous anesthetic agent that commonly induces significant neuroapoptosis. MicroRNAs (miRNAs) have been reported to participate in the regulation of propofol exposure-mediated neurotoxicity. The mechanism through which miRNAs regulate propofol exposure-mediated neurotoxicity is still unclear. Increasing evidences have shown that miRNAs are involved in the regulation of propofol exposure-mediated neurotoxicity. MiR-215 is reduced in ischemic stroke, which leads to suppression of nerve cell apoptosis, autophagy, ischemic infarction and improved neurological deficit via down-regulation of nuclear factor-κB activator 1/ interleukin-17 receptor A pathway. These results suggest that miR-215 plays a neuroprotective role in ischemic injury (Sun et al 2018). The role of miR-215 in propofol exposure-induced neurotoxicity is still unclear
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