English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The present study aimed to investigate the effects of microRNA (miR)‑214 on neuroapoptosis induced by propofol and the possible mechanism of its anti‑apoptotic effects. Initially, it was observed that miR‑214 expression was upregulated in propofol‑induced neuroapoptosis rats. Next, propofol‑treated nerve cells were transfected with miR‑214 mimics. The results revealed that miR‑214 overexpression induced apoptosis, inhibited cell proliferation, inhibited cyclin D1 protein expression, promoted caspase‑3 activity and B‑cell lymphoma 2‑associated X protein expression, and enhanced the levels of inflammation factors in nerve cells treated with propofol. In addition, miR‑214 overexpression suppressed phosphoinositide 3‑kinase/protein kinase B (PI3K/Akt) signaling by targeting the activation of phosphatase and tensin homolog (PTEN) and nuclear factor‑κB expression in nerve cells treated with propofol. Treatment with a PTEN inhibitor successfully suppressed the PTEN protein expression and decreased the apoptosis of propofol‑treated nerve cells subsequent to miR‑214 overexpression through PI3K/Akt signaling. In conclusion, the present study data revealed that miR‑214 suppressed propofol‑induced neuroapoptosis through the activation of PI3K/Akt signaling by targeting PTEN expression.

international journal of molecular medicine

MicroRNA‑214 suppresses propofol‑induced neuroapoptosis through activation of phosphoinositide 3‑kinase/protein kinase B signaling by targeting phosphatase and tensin homolog expression