EGCG's Protective Role Against Brain Cell Death in 3D Human Glial Cell Model of Alzheimer's Disease
Seunghyun Cho
Korea International School, Jeju, Korea
Publication date: May 31, 2025
Korea International School, Jeju, Korea
Publication date: May 31, 2025
DOI: http://doi.org/10.34614/JIYRC2025I09
ABSTRACT
Epigallocatechin gallate (EGCG) is a natural substance from green tea, known for its anti-ROS (reactive oxygen species) properties. This study aimed to investigate the protective effect of EGCG against Scopolamine hydrobromide (SH)-induced cell death and intracellular ROS levels in a human glial cell lines model of Alzheimer's Disease. Our findings indicate that 50 µM SH effectively induced cell death in A172 human glial cells, providing a reliable model for mimicking Alzheimer's disease pathology. However, post-treatment with EGCG significantly protected against SH-induced cell death, as evidenced by enhanced cell viability. Additionally, EGCG treatment effectively reduced intracellular ROS levels, as shown by the decreased green fluorescence intensity in the fluorescence microscopy images. The quantification of intracellular ROS levels further supported the effectiveness of EGCG in mitigating SH-induced oxidative stress. Also, cells subjected to 50 µM SH followed by EGCG treatment demonstrate the protection of A172 cells within the 3D culture model. These results highlight the potential of EGCG as a neuroprotective agent in Alzheimer's disease, as it not only promotes cell viability but also reduces intracellular ROS levels. The ability of EGCG to modulate these crucial factors suggests its potential as a therapeutic intervention for protecting glial cells and combating the progression of Alzheimer's pathology.
Epigallocatechin gallate (EGCG) is a natural substance from green tea, known for its anti-ROS (reactive oxygen species) properties. This study aimed to investigate the protective effect of EGCG against Scopolamine hydrobromide (SH)-induced cell death and intracellular ROS levels in a human glial cell lines model of Alzheimer's Disease. Our findings indicate that 50 µM SH effectively induced cell death in A172 human glial cells, providing a reliable model for mimicking Alzheimer's disease pathology. However, post-treatment with EGCG significantly protected against SH-induced cell death, as evidenced by enhanced cell viability. Additionally, EGCG treatment effectively reduced intracellular ROS levels, as shown by the decreased green fluorescence intensity in the fluorescence microscopy images. The quantification of intracellular ROS levels further supported the effectiveness of EGCG in mitigating SH-induced oxidative stress. Also, cells subjected to 50 µM SH followed by EGCG treatment demonstrate the protection of A172 cells within the 3D culture model. These results highlight the potential of EGCG as a neuroprotective agent in Alzheimer's disease, as it not only promotes cell viability but also reduces intracellular ROS levels. The ability of EGCG to modulate these crucial factors suggests its potential as a therapeutic intervention for protecting glial cells and combating the progression of Alzheimer's pathology.
