Neuroprotective effects of cerebroprotein hydrolysate and its combination with antioxidants against oxidative stress-induced HT22 cell death.

This study aimed to investigate the neuroprotective effects of cerebroprotein hydrolysate (CPH) against oxidative stress-induced HT22 cell death. Additionally, the effect of antioxidants such as quercetin (QC) and N-acetyl-L-cysteine (NAC) on the neuroprotective activity of CPH was evaluated. The mouse-derived hippocampal neuronal cell line HT22 was pretreated with CPH or a mixture of CPH and QC or NAC. HT22 cell death was induced by either 10 mM glutamate, 2.5 μM amyloid-β (Aβ)(25-35), and 300 μM cobalt chloride (CoCl(2)). As results, CPH effectively alleviated HT22 cell death induced by glutamate, Aβ(25-35), and CoCl(2). In addition, CPH combination with QC augmented cell viability in both glutamate- and Aβ(25-35)-stressed conditions but had no synergic effect on the CoCl(2)-stressed condition. The synergic effect of CPH and NAC combination was observed under all cell death conditions. The neuroprotective actions of CPH and its combinations with QC or NAC against various oxidative stress-induced HT22 cell deaths were demonstrated, providing a promising strategy for developing CPH preparations for the prevention and/or treatment of neurodegenerative diseases such as Alzheimer's disease.