Theasinensins A Against Methylglyoxal‐Induced Neurotoxicity via Autophagy in SH‐SY5Y Cells

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 polyphenols have notable effects against various types of cancers, blood pressure, cardiovascular problems, arthritis, and atherosclerosis without inducing major toxicity consequences. Tea polyphenols have a role in the reversal of age‐related loss of neuronal plasticity and recovery after neuronal lesions. Theasinensins are a group of tea polyphenols different from green tea catechins, and they are considered as bioactive compounds in Oolong tea. During enzymatic oxidation, EGCG is fermentated and several B‐ring homodimers: theasinensins A (TSA) intermediates generated. TSA had been found to have many bioactivities, such as anti‐oxidation. However, the effect of the neuroprotective effect of this tea polyphenol remains unclear. The aim of this study is to investigate the neuroprotective effects and the molecular mechanism of TSA against MG‐induced toxicity in SH‐SY5Y cell model. The cell viability assay demonstrated that TSA treatment protected cells from MG‐induced neurotoxicity. The result of acridine orange (AO) stain, detecting AO fluoresce intensity and the level of LC3, showed that TSA could increase intracellular AVO value and induce autophagy in MG‐treated neuron cell. We expect that TSA could be reagents to protect neurodegenerative diseases. Support or Funding Information This study was supported by NSC 100‐2313‐B‐309‐003 to A‐C Cheng This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .