The Protective Effect of Tea Polyphenol against Methylglyoxal-induced Neurotoxicity

• Main Authors: Tzu-Li Huang, 黃孜立
• Other Authors: Min-Hsiung Pan
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/94247773181314123932

碩士 === 國立臺灣大學 === 食品科技研究所 === 104 === Methylglyoxal (MG) is a highly reactive dicarbonyl aldehyde. MG has been proved to be toxic to neuron and may be the reason of many neurodegenerative diseases. Tea is a traditional drinking and previous studies have observed that chronic tea consumption may reduce the risk of neurodegeneration. One of the most well-known tea catechin, (-)-epigallocatechin-3-gallate (EGCG), and theasinensin A (TSA), the dimer of EGCG had been found to have many bioactivities, such as anti-oxidation. However, the effect of the neuroprotective effect of tea polyphenol remains unclear. The aim of this study is to investigate the neuroprotective effects and the molecular mechanism of tea polyphenol against MG-induced toxicity in SH-SY5Y cell model. The cell viability assay demonstrated that EGCG and TSA treatment protected cells from MG-induced neurotoxicity. Besides, evidences from flow cytometry showed that EGCG and TSA inhibited MG-induced oxidative stress via reducing MG-induced reactive oxygen species (ROS) generation and induce intracellular GSH level. Through activation of caspase 3 and cleavage-PARP, EGCG would inhibit MG-induced apoptosis but TSA did not inhibit MG-induced apoptosis. The result of acridine orange (AO) stain, detecting AO fluoresce intensity and the level of LC3, showed that TSA would induce autophagy in MG-treated neuron cell. EGCG inhibited p53 and MAPK pathway to increase cell viability via western blotting analysis; on the other hand, TSA inhibited Akt pathway to induce autophagy. In conclusion, both EGCG and TSA has the ability to protect cell from MG-induced cytotoxicity via different mechanisms. We expect that EGCG and TSA could be reagents to protect neurodegenerative diseases.