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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  μ M), HIP (2  μ M), or EGT + HIP, then challenged with MGO under high-glucose condition (30  μ M 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  μ M 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- κ B) 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- κ B transcription pathway through antioxidant activities.

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