Abstract
It is well-established that amyloid β (Aβ)-induced oxidative stress plays a crucial role in Alzheimer's disease (AD) and its cognitive deficits. HX106N is a water-soluble extract prepared from a mixture of the plants Dimocarpus longan, Liriope platyphylla, Salvia miltiorrhiza, and Gastrodia elata. These ingredients are traditionally used in various plant-based medicines for the treatment of neurological disease. In this study, we examined the effects of HX106N on memory impairment and oxidative stress caused by the intracerebroventricular injection of Aβ25–35 peptide in mice. For one week prior to Aβ25–35 peptide injection and 8 days after, mice were given oral HX106N. HX106N treatment reversed the Aβ25–35-mediated decrease in alternation percentage and latency time in the Y-maze and passive avoidance tests. Mice treated with HX106N showed decreased levels of thiobarbituric acid reactive substances (TBARS), a lipid peroxidation marker. Quantitative RT-PCR demonstrated that HX106 treatment increased levels of heme oxygenase-1 (HO-1) in the hippocampus of Aβ25–35-injected mice, while having little effect on the expression of TNF-α and IL-1β. In the murine hippocampal neuronal cell line HT22, HX106N was found to upregulate HO-1 expression at the RNA and protein levels as well as to protect cells from glutamate-induced oxidative stress. Taken together, our data suggest that HX106N may potentially act as a preventive and/or therapeutic agent for AD.
