Related Experiment Video

Updated: May 19, 2026

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization
10:45

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization

Published on: January 13, 2012

Propofol and magnesium attenuate isoflurane-induced caspase-3 activation via inhibiting mitochondrial permeability

Yiying Zhang1, Yuanlin Dong, Zhipeng Xu

  • 1Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St, Room 4310, Charlestown, MA, 02129-2060, USA. zxie@partners.org.

Medical Gas Research
|August 21, 2012
PubMed
Abstract

Insights

Magnesium and propofol may protect against isoflurane anesthesia neurotoxicity. These agents block the mitochondrial permeability transition pore (mPTP), reducing isoflurane-induced cell damage and caspase activation.

Area of Science:

  • Neuroscience
  • Anesthesiology
  • Mitochondrial Biology

Background:

  • Inhalation anesthetic isoflurane can induce apoptosis via mitochondrial permeability transition pore (mPTP) opening, potentially impairing learning and memory.
  • Cyclosporine A, magnesium, and propofol are known mPTP blockers.

Purpose of the Study:

  • To investigate if propofol and magnesium can attenuate isoflurane-induced caspase activation and mPTP opening.
  • To explore potential neuroprotective strategies against anesthetic-induced toxicity.

Main Methods:

  • Utilized H4 human neuroglioma cells expressing amyloid precursor protein (APP) and six-day-old wild-type mice.
  • Assessed mPTP opening and caspase activation using Western blot analysis and flow cytometry.
  • Examined the effects of magnesium sulfate (Mg2+), propofol, and isoflurane.

Main Results:

  • Magnesium (Mg2+) and propofol significantly attenuated isoflurane-induced caspase-3 activation in both cell cultures and mouse brain tissue.
  • Both Mg2+ and propofol mitigated isoflurane-induced mPTP opening in H4 APP cells.
  • These findings demonstrate the inhibitory effects of Mg2+ and propofol on isoflurane-induced mitochondrial dysfunction.

Conclusions:

  • Magnesium and propofol may ameliorate isoflurane-induced neurotoxicity by inhibiting mitochondrial dysfunction.
  • These results suggest potential therapeutic applications for Mg2+ and propofol in preventing and treating anesthesia-related neurotoxicity.
  • Further research is warranted to validate these findings in clinical settings.

More Related Videos

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction08:41

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction

Published on: January 12, 2016

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Related Concept Videos

Parenteral Anesthetics: Overview01:24

Parenteral Anesthetics: Overview

Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.