베타아밀로이드로 유도된 신경세포 사멸에 대한 고려홍삼의 보호효과 연구

• Published in: 大韓本草學會誌 Vol. 40; no. 4; pp. 73 - 81
• Main Authors: 박규환, Gyu Hwan Park, 장정희, Jung-hee Jang
• Format: Journal Article
• Language: Korean
• Published: 대한본초학회 31.07.2025
• Subjects: Alzheimer’s disease; antioxidant defense; Korean red ginseng; neuroprotection; oxidative damages; β-amyloid; 한의학; oxidative damages; antioxidant defense; Korean red ginseng; Alzheimer's disease; neuroprotection; {\beta}$-amyloid
• ISSN: 1229-1765; 2288-7199
• DOI: 10.6116/kjh.2025.40.4.73

Objectives : This study aimed to investigate the neuroprotective effects and underlying molecular mechanisms of Korean Red Ginseng extract (RGE) against β-amyloid (Aβ25-35)-induced oxidative cell death in SH-SY5Y human neuroblastoma cells. Methods : The protective effects of RGE against Aβ-induced oxidative cell death were assessed using MTT assay for cell viability and TUNEL staining for apoptotic DNA fragmentation. Mitochondrial membrane potential disruption and expression levels of apoptosis-related proteins (Bax, Bcl-2, cleaved PARP) and stress-activated kinase JNK were evaluated. Oxidative stress markers, including intracellular reactive oxygen species (ROS) accumulation and lipid peroxidation, were measured. To determine antioxidant mechanisms, levels of reduced glutathione (GSH) and expression of antioxidant enzymes (γ-glutamylcysteine ligase, heme oxygenase-1, catalase, and superoxide dismutase) were analyzed by reverse transcription-polymerase chain reaction. Results : RGE significantly attenuated Aβ-induced apoptotic cell death, evidenced by reduced DNA fragmentation, preserved mitochondrial membrane potential, decreased Bax/Bcl-2 ratio, and suppression of JNK activation and PARP cleavage. RGE also inhibited Aβ-induced oxidative stress by reducing intracellular ROS accumulation and lipid peroxidation. Furthermore, RGE enhanced cellular antioxidant defense by increasing GSH content and upregulating the expression of key antioxidant enzymes. Notably, RGE selectively modulated the HO-1, catalase, and GCLC pathways without significantly affecting superoxide dismutase, suggesting targeted modulation of distinct antioxidant pathways. Conclusions : These findings suggest that RGE exerts neuroprotective effects against Aβ-induced oxidative neuronal injury by suppressing apoptosis and enhancing endogenous antioxidant defense systems. RGE holds potential as a therapeutic candidate for the prevention and treatment of Alzheimer’s disease.