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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 consistently protected. Baicalin inhibited Aβ-induced neuronal apoptosis via multiple targets and multiple pathways, such as the inhibition of free radical damage, reduction of caspa se-3 expression, and protection of normal mitochondrial functions.