Protective effects of baicalin on amyloid beta 25-35- induced apoptosis in human neuroblastoma SH-SY5Y cells

• Published in: Neural regeneration research Vol. 5; no. 22; pp. 1739 - 1744
• Main Author: Miao Geng Hongyan Chen Jianhua Wang Yazhuo Hu Jianwei Liu Jing Liu Jingkun Pan Yuhong Gao
• Format: Journal Article
• Language: English
• Published: Institute of Geriatrics, Division of South Building, Chinese PLA General Hospital, Beijing 100853, China 30.11.2010
• Subjects: caspase; β淀粉样蛋白; 保护机制; 神经母细胞瘤; 神经细胞凋亡; 线粒体膜电位; 黄芩苷; neural regeneration; baicalin; amyloid β; neuron; apoptosis; traditional Chinese medicine; caspase-3
• ISSN: 1673-5374
• DOI: 10.3969/j.issn.1673-5374.2010.22.010

Baicalin, a type of flavanoid, effectively prevents cellular apoptosis induced by various factors. However, little evidence is available regarding its role on amyloid β （Aβ） -induced neuronal apoptosis. The present study investigated the protective mechanisms of baicalin on Aβ-induced neuronal apoptosis. Flow cytometry and cation dye 5, 5＇, 6, 6＇-tetrachloro-1, 1＇, 3, 3＇-tetraethyl- benzimidazoly lcarbocyanine iodide （JC-1） were employed to measure mitochondrial membrane potential, and nitric oxide secretion and apoptotic-related factors, such as caspase-3, were comprehensively analyzed. Results demonstrated a protective effect of baicalin on Aβ-treated SH-SY5Y cell viability; the rate of apoptosis decreased, nitric oxide generation and expression of caspase-3 were effectively inhibited, and mitochondrial membrane potential was effectively protected. Baicalin inhibited Aβ-induced neuronal apoptosis via multiple targets and multiple pathways, such as the inhibition of free radical damage, reduction of caspase-3 expression, and protection of normal mitochondrial functions.