Escitalopram Partially Rescues Cortisol-Induced Stress in Human Glial Cells: Morphological and Viability-Based Evidence
Jiyoon Shin
Cornerstone Collegiate Academy of Seoul, Seoul, South Korea
Publication date: July 19, 2026
Cornerstone Collegiate Academy of Seoul, Seoul, South Korea
Publication date: July 19, 2026
DOI: http://doi.org/10.34614/JIYRC2026I39
ABSTRACT
Depression is a rising major psychiatric disorder, and dysregulation of the Hypothalamic–Pituitary–Adrenal (HPA) axis due to the stress hormone cortisol has been proposed as a key biological mechanism indicating its pathophysiology. Particularly, glial cells play a crucial role in maintaining neural homeostasis and regulating stress responses. Therefore, establishing a cellular-level stress model is essential for understanding the mechanisms of antidepressant action. This study aimed to investigate cortisol-induced cellular damage in human-derived glial cells and to evaluate whether escitalopram oxalate, a selective serotonin reuptake inhibitor (SSRI), could recover these stress-related effects. Glial cells were treated with each cortisol and escitalopram in a concentration range of 0-300 µL, then were analyzed by brightfield microscopic observation and quantitative cell viability analysis. The results showed that cortisol-induced dose-dependent morphological changes and reductions in cell viability. Nevertheless, escitalopram significantly increased cell viability at an intermediate concentration (200 µL) and partially restored viability when cortisol was exposed. In conclusion, these findings suggest that escitalopram may exert a partial cytoprotective effect against cortisol-induced glial stress and are meaningful in that they reemerge the stress-depression correlation at the cellular level.
Depression is a rising major psychiatric disorder, and dysregulation of the Hypothalamic–Pituitary–Adrenal (HPA) axis due to the stress hormone cortisol has been proposed as a key biological mechanism indicating its pathophysiology. Particularly, glial cells play a crucial role in maintaining neural homeostasis and regulating stress responses. Therefore, establishing a cellular-level stress model is essential for understanding the mechanisms of antidepressant action. This study aimed to investigate cortisol-induced cellular damage in human-derived glial cells and to evaluate whether escitalopram oxalate, a selective serotonin reuptake inhibitor (SSRI), could recover these stress-related effects. Glial cells were treated with each cortisol and escitalopram in a concentration range of 0-300 µL, then were analyzed by brightfield microscopic observation and quantitative cell viability analysis. The results showed that cortisol-induced dose-dependent morphological changes and reductions in cell viability. Nevertheless, escitalopram significantly increased cell viability at an intermediate concentration (200 µL) and partially restored viability when cortisol was exposed. In conclusion, these findings suggest that escitalopram may exert a partial cytoprotective effect against cortisol-induced glial stress and are meaningful in that they reemerge the stress-depression correlation at the cellular level.
