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Background <p>Propofol (PPF) is one of the most widely used intravenous anesthetics in clinical practice and has neuroprotective effects. Ropivacaine (RVC) is a local anesthetic that may induce neurotoxicity.</p> Objectives <p>This study aims to investigate the effect of PPF on RVC-induced neurotoxicity.</p> Results <p>RVC inhibited cell viability, increased LDH release and ROS levels, and promoted cell apoptosis, leading to neurotoxicity in SK-N-SH cells. PPF alleviated RVC-induced neurotoxicity by increasing cell viability, decreasing LDH release and ROS levels, inhibiting cell apoptosis, and downregulating MALAT1 expression. MALAT1 recruited EZH2 to increase H3K27me3 modification, thereby suppressing BDNF expression. Overexpression of MALAT1 or inhibition of BDNF partially reversed the protective effect of PPF on RVC-induced neurotoxicity.</p> Conclusions <p>PPF downregulates MALAT1 expression in RVC-induced neurotoxicity, inhibits the recruitment of EZH2 to reduce H3K27me3 modification, and promotes BDNF expression, thereby exerting neuroprotective effects.</p>

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Propofol alleviates ropivacaine-induced neurotoxicity through the MALAT1/EZH2/BDNF axis

  • 期刊论文

  • 发表日期：

    2025年1月17日

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  • Xiaoqing Liu,
  • Chun Chen

摘要

Background

Propofol (PPF) is one of the most widely used intravenous anesthetics in clinical practice and has neuroprotective effects. Ropivacaine (RVC) is a local anesthetic that may induce neurotoxicity.

Objectives

This study aims to investigate the effect of PPF on RVC-induced neurotoxicity.

Results

RVC inhibited cell viability, increased LDH release and ROS levels, and promoted cell apoptosis, leading to neurotoxicity in SK-N-SH cells. PPF alleviated RVC-induced neurotoxicity by increasing cell viability, decreasing LDH release and ROS levels, inhibiting cell apoptosis, and downregulating MALAT1 expression. MALAT1 recruited EZH2 to increase H3K27me3 modification, thereby suppressing BDNF expression. Overexpression of MALAT1 or inhibition of BDNF partially reversed the protective effect of PPF on RVC-induced neurotoxicity.

Conclusions

PPF downregulates MALAT1 expression in RVC-induced neurotoxicity, inhibits the recruitment of EZH2 to reduce H3K27me3 modification, and promotes BDNF expression, thereby exerting neuroprotective effects.