★ Oxidative stress induced by Aβ25–35 could be inhibited by HBO and EGB761. ★ The mitochondria-mediated apoptosis signaling way could be inhibited by HBO and EGB761. ★ The combined treatment of HBO and Ginkgo showed better effects.
Alzheimer's disease (AD) is characterized by accumulation and deposition of Aβ peptides in human brains. The present study aimed to determine the protective effect of HBO and EGB761 on Aβ25–35 peptides induced cognitive impairment and neuronal toxicity in rats. Characteristics of AD were induced in rats by the administration of Aβ25–35 in hippocampus. Rats were treated with HBO (2ATA 60 min/day), EGB761 (20 mg/kg/day), and the combination of HBO + EGB761 (20 mg/kg/day + 2ATA). The Morris water maze was used to detect the protective effects of HBO and EGB761 against cognitive impairment. The activities of SOD and GSH, the apoptosis-related genes and proteins and the apoptosis rate of hippocampus were detected. Compared to the model group, EGB761 and HBO treatments synergistically improved the escape latency. Furthermore, the activities of SOD and GSH in rat hippocampal tissue were found to have increased with a concomitant reduction in MDA levels, Bax expression, cytochrome c release, and the activity of caspase-9/3. Accordingly, a significant reduction was observed in the apoptosis rate following the treatment with EGB761 and HBO in this model of AD. Our findings suggest that HBO and EGB761 reduce cell toxicity and oxidative stress by blocking mitochondria-mediated apoptosis signaling in AD, and the combined treatment of HBO and Ginkgo further enhances these effects.