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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 4824371, 10 pages
Research Article

Protective Effects and Possible Mechanisms of Ergothioneine and Hispidin against Methylglyoxal-Induced Injuries in Rat Pheochromocytoma Cells

1Department of Bioindustry Technology, Da-Yeh University, Dacun, Taiwan
2Department of Nutrition, Chung Shan Medical University Hospital, Taichung, Taiwan

Correspondence should be addressed to Tuzz-Ying Song; wt.ude.uyd.liam@77gnos

Received 6 June 2017; Revised 8 August 2017; Accepted 23 August 2017; Published 17 October 2017

Academic Editor: Mohamed M. Abdel-Daim

Copyright © 2017 Tuzz-Ying Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetic encephalopathy (DE) is often a complication in patients with Alzheimer’s disease due to high blood sugar induced by diabetic mellitus. Ergothioneine (EGT) and hispidin (HIP) are antioxidants present in Phellinus linteus. Methylglyoxal (MGO), a toxic precursor of advanced glycated end products (AGEs), is responsible for protein glycation. We investigated whether a combination EGT and HIP (EGT + HIP) protects against MGO-induced neuronal cell damage. Rat pheochromocytoma (PC12) cells were preincubated with EGT (2 μM), HIP (2 μM), or EGT + HIP, then challenged with MGO under high-glucose condition (30 μM MGO + 30 mM glucose; GLU + MGO) for 24–96 h. GLU + MGO markedly increased protein carbonyls and reactive oxygen species in PC12 cells; both of these levels were strongly reduced by EGT or HIP with effects comparable to those of 100 nM aminoguanidine (an AGE inhibitor) but stronger than those of 10 μM epalrestat (an aldose reductase inhibitor). GLU + MGO significantly increased the levels of AGE and AGE receptor (RAGE) protein expression of nuclear factor kappa-B (NF-κB) in the cytosol, but treatment with EGT, HIP, or EGT + HIP significantly attenuated these levels. These results suggest that EGT and HIP protect against hyperglycemic damage in PC12 cells by inhibiting the NF-κB transcription pathway through antioxidant activities.