Kaempferol, Quercetin 및 그 배당체의 Hydrogen Peroxide에 의한 신경세포의 산화적 스트레스 보호 효과

초록

Oxidative stress in the brain is a well-known cause of neurodegenerative diseases including Alzheimer’s disease. In the present study, we investigated the protective effects of flavonoids such as kaempferol (K), quercetin (Q), kaempferol-3-O-glucoside (KG), and quercetin-3-β-Dglucoside (QG) from oxidative stress induced by H2O2 in SH-SY5Y neuronal cells. Cell viability was confirmed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. To examine the neuroprotective mechanism, we measured the expression of apoptosis-related proteins such as caspase-3, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) using western blotting. Compared with normal cells, treatment with H2O2 significantly decreased cell viability, whereas treatment with the four flavonoids increased cell viability compared with that of H2O2-treated control cells. In particular, treatment with Q led to an increase in cell viability from 65.32% to 94.37%, which was the strongest protective effect observed among the flavonoids. In addition, H2O2-treated cells induced apoptosis by upregulating cleaved caspase-3 and Bax and downregulating Bcl-2. However, flavonoid treatment attenuated neuronal apoptosis by regulating apoptosis-related factors. Kaempferol-3-O-glucoside attenuated apoptosis by inhibiting Bax expression. Compared with the H2O2-treated control group, treatment with Q and QG downregulated the expression of pro-apoptotic proteins, such as cleaved caspase-3 and Bax. The results of this study indicate that the four flavonoids, K, KG, Q, and QG, attenuate H2O2-induced oxidative stress by regulating apoptosis-related factors in SH-SY5Y neuronal cells, suggesting that they are promising agents for oxidative stress-related neurodegenerative diseases.

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