摘要
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.
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.
基金
the Chinese PLA General Hospital Nursery Fund,No.07MP417
