Hyperbaric Oxygen and Ginkgo Biloba Extract Ameliorate Cognitive and Memory Impairment via Nuclear Factor Kappa-B Pathway in Rat Model of Alzheimer’s Disease.
Hyperbaric oxygen (HBO) and Ginkgo biloba extract (e.g., EGB 761) were shown to ameliorate cognitive and memory impairment in Alzheimer’s disease (AD). However, the exact mechanism remains elusive. The aim of the present study was to investigate the possible mechanisms of HBO and EGB 761 via the function of nuclear factor kappa-B (NF-κB) pathway. AD rats were induced by injecting β-amyloid 25-35 into the hippocampus. All animals were divided into six groups: Normal, sham, AD model, HBO (2 atmosphere absolute; 60 min/d), EGB 761 (20 mg·kg-1·d-1 ), and HBO/EGB 761 groups. Morris water maze tests were used to assess cognitive, and memory capacities of rats; TdT-mediated dUTP Nick-End Labeling staining and Western blotting were used to analyze apoptosis and NF-κB pathway-related proteins in hippocampus tissues. orris water maze tests revealed that EGB 761 and HBO significantly improved the cognitive and memory ability of AD rats. In addition, the protective effect of combinational therapy (HBO/EGB 761) was superior to either HBO or EGB 761 alone. In line, reduced apoptosis with NF-κB pathway activation was observed in hippocampus neurons treated by HBO and EGB 761. ur results suggested that HBO and EGB 761 improve cognitive and memory capacity in a rat model of AD. The protective effects are associated with the reduced apoptosis with NF-κB pathway activation in hippocampus neurons.
The protective effect of hyperbaric oxygen and Ginkgo biloba extract on Aβ25-35-induced oxidative stress and neuronal apoptosis in rats.
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 60min/day), EGB761 (20mg/kg/day), and the combination of HBO+EGB761 (20mg/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.
Hyperbaric oxygen and Ginkgo Biloba extract inhibit Aβ25-35-induced toxicity and oxidative stress in vivo: a potential role in Alzheimer’s disease.
Alzheimer’s disease is characterized by the accumulation and deposition of Aβ peptides in human brains and Aβ induced free radical-mediated damage is one of the hypotheses. In the present study, we explored the protective effects of hyperbaric oxygen (HBO) and Ginkgo Biloba extract (EGB761) on Aβ25-35-induced brain toxicity. Our results demonstrated that EGB761, HBO, and the combination HBO and EGB761, could significantly improve the cognitive function in AD rats’ model, especially the combination group. What’s more, the activities of superoxide dismutase (SOD) in rat hippocampal tissue were obviously enhanced followed by evidently reduced malondialdehyde (MDA) levels in the same treatment groups mentioned earlier. There were no differences of nitric oxide (NO) productions in the group of EGB761, HBO, and HBO and EGB761, but they were all lower than that of model group. These findings suggest that both HBO and EGB761 may relieve cell toxicity and oxidative stress in AD and thus play a potential protective role in AD. Furthermore, the combination could have better effects compared with single one.