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Updated: Jun 23, 2026
Measuring Membrane Lipid Turnover with the pH-sensitive Fluorescent Lipid Analog ND6
Published on: July 29, 2021
Descriptive oxidative and lipid-related fluorescence observations associated with Esketamine treatment in a
Xinzhe Ni1, Shuting Zhou1, Xudong He1
1College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China.
Background:
In HT-22 cells, 500 μM NMDA was used as a high-concentration oxidative stressor rather than a classical NMDA receptor-mediated excitotoxic stimulus. Because HT-22 cells lack functional ionotropic NMDA receptors, this model cannot test NMDA receptor antagonist-mediated pharmacology.
Methods:
HT-22 cells and C8-D1A astrocytes were examined in a Transwell co-culture system. CCK-8 viability readout, ApoE Western blot signal, lipid peroxidation, BODIPY C12-associated fluorescence, TOMM20-region BODIPY C12 fluorescence, and MitoSOX fluorescence were assessed.
Results:
NMDA exposure was associated with a lower CCK-8 viability readout and higher lipid peroxidation fluorescence. Esketamine treatment was associated with a higher CCK-8 viability readout and lower lipid peroxidation fluorescence under these oxidative stress conditions. In co-cultured astrocytes, NMDA-challenged HT-22 cells were associated with increased lipid peroxidation, altered BODIPY C12-associated fluorescence, and elevated MitoSOX fluorescence, whereas these signals were lower in the esketamine-treated condition. ApoE changes were descriptive and were not used to infer mechanism. The source and molecular identity of astrocytic BODIPY C12-associated fluorescence remain uncertain.
Conclusions:
Esketamine-associated effects in this model should be interpreted as receptor-independent, oxidative-stress-associated viability and fluorescence observations. The findings are descriptive and hypothesis-generating and do not establish direct lipid transfer, causal metabolic coupling, mitochondrial fatty-acid utilization, or a defined lipid-metabolic mechanism.
