蓮根의 신경 보호 효과 및 기전연구
The Mechanism of Lotus Root Extract (LRE) as Neuro-Protective Effect in Alzheimer Disease (AD)
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초록
Objectives :There is a possibility LRE as remedy in Alzheimer disease (AD), but it’s nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on Aβ25-35 pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods :We tried to confirm that effect by experimenting with 20, 50, and 100μg/ml concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced Aβ25-35, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under H2O2 treatment condition in a SH-SY5Y cell.Results :1. In Aβ25-35 treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued Aβ25-35 and oxidative stress, modify JNK engaged synaptic structure and NFκB induced p75-neurotrophin receptor polymorphism.Conclusions :We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of Aβ25-35 treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for Aβ25-35 clearance and as scavenger for active oxygen free radical.
Abstract
Objectives :There is a possibility LRE as remedy in Alzheimer disease (AD), but it’s nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on Aβ25-35 pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods :We tried to confirm that effect by experimenting with 20, 50, and 100μg/ml concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced Aβ25-35, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under H2O2 treatment condition in a SH-SY5Y cell.Results :1. In Aβ25-35 treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued Aβ25-35 and oxidative stress, modify JNK engaged synaptic structure and NFκB induced p75-neurotrophin receptor polymorphism.Conclusions :We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of Aβ25-35 treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for Aβ25-35 clearance and as scavenger for active oxygen free radical.
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