|
KMID : 0043320190420121081
|
|
Archives of Pharmacal Research
2019 Volume.42 No. 12 p.1081 ~ p.1091
|
|
|
Protective effects of 6,7,4′-trihydroxyisoflavone, a major metabolite of daidzein, on 6-hydroxydopamine-induced neuronal cell death in SH-SY5Y human neuroblastoma cells
|
|
Ko Yong-Hyun
Kwon Seung-Hwan
Kim Seon-Kyung
Lee Bo-Ram
Hur Kwang-Hyun
Kim Young-Jung
Kim Seong-Eon
Lee Seok-Yong
Jang Choon-Gon
|
|
|
Abstract
|
|
|
|
Daidzein, one of the important isoflavones, is extensively metabolized in the human body following consumption. In particular, 6,7,4′-trihydroxyisoflavone (THIF), a major metabolite of daidzein, has been the focus of recent investigations due to its various health benefits, such as anti-cancer and anti-obesity effects. However, the protective effects of 6,7,4′-THIF have not yet been studied in models of Parkinson’s disease (PD). Therefore, the present study aimed to investigate the protective activity of 6,7,4′-THIF on 6-hydroxydopamine (OHDA)-induced neurotoxicity in SH-SY5Y human neuroblastoma cells. Pretreatment of SH-SY5Y cells with 6,7,4′-THIF significantly inhibited 6-OHDA-induced neuronal cell death, lactate dehydrogenase release, and reactive oxygen species production. In addition, 6,7,4′-THIF significantly attenuated reductions in 6-OHDA-induced superoxide dismutase activity and glutathione content. Moreover, 6,7,4′-THIF attenuated alterations in Bax and Bcl-2 expression and caspase-3 activity in 6-OHDA-induced SH-SY5Y cells. Furthermore, 6,7,4′-THIF significantly reduced 6-OHDA-induced phosphorylation of c-Jun N-terminal kinase, p38 mitogen-activated protein kinase, and extracellular signal-regulated kinase 1/2. Additionally, 6,7,4′-THIF effectively prevented 6-OHDA-induced loss of tyrosine hydroxylase. Taken together, these results suggest that 6,7,4′-THIF, a major metabolite of daidzein, may be an attractive option for treating and/or preventing neurodegenerative disorders such as PD.
|
|
|
KEYWORD
|
|
|
6,7,4′-Trihydroxyisoflavone, 6-Hydroxydopamine, Oxidative stress, Apoptosis, Parkinson’s disease
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
  
|
|