Investigating the Neuroprotective and Stress-Modulating Effects of Oxytocin on Human Cells under Cortisol-Induced Stress Conditions
Seoyeon Lee
The Taft School, Waterbury, United States
Publication date: November 20, 2025
The Taft School, Waterbury, United States
Publication date: November 20, 2025
DOI: http://doi.org/10.34614/JIYRC2025II16
ABSTRACT
Cortisol, a primary stress hormone, is known to impair neuronal health and disrupt pathways essential for emotional regulation and social bonding. This study aimed to investigate whether oxytocin can mitigate the cortisol-induced cellular damage in human glial A172 cells by observing the expression of oxytocin receptor (OR) and brain-derived neurotrophic factor (BDNF), both linked to prosocial behavior and neuroplasticity. Cells were treated with 1 μM cortisol, 3 μM oxytocin, or co-treated with 1 μM cortisol and 3 μM oxytocin, also including a control group. Immunofluorescence staining was performed to visualize OR and BDNF expression, followed by a quantification of fluorescence intensity. Despite a relatively minor dose, cortisol treatment markedly reduced OR and BDNF signals, whereas oxytocin co-treatment resulted in widespread, intense fluorescence, with OR expression increasing over 3.5-fold (p = 0.0015) and BDNF also significantly elevated. These results suggest that oxytocin can buffer cortisol’s detrimental effects, potentially preserving social connectivity and emotional resilience, and highlight its promise as a target for interventions in stress-related social impairments.
Cortisol, a primary stress hormone, is known to impair neuronal health and disrupt pathways essential for emotional regulation and social bonding. This study aimed to investigate whether oxytocin can mitigate the cortisol-induced cellular damage in human glial A172 cells by observing the expression of oxytocin receptor (OR) and brain-derived neurotrophic factor (BDNF), both linked to prosocial behavior and neuroplasticity. Cells were treated with 1 μM cortisol, 3 μM oxytocin, or co-treated with 1 μM cortisol and 3 μM oxytocin, also including a control group. Immunofluorescence staining was performed to visualize OR and BDNF expression, followed by a quantification of fluorescence intensity. Despite a relatively minor dose, cortisol treatment markedly reduced OR and BDNF signals, whereas oxytocin co-treatment resulted in widespread, intense fluorescence, with OR expression increasing over 3.5-fold (p = 0.0015) and BDNF also significantly elevated. These results suggest that oxytocin can buffer cortisol’s detrimental effects, potentially preserving social connectivity and emotional resilience, and highlight its promise as a target for interventions in stress-related social impairments.
