Hyperbaric Oxygen and Ginkgo Biloba Extract Ameliorate Cognitive and Memory Impairment via Nuclear Factor Kappa-B Pathway in Rat Model of Alzheimer's Disease.

BACKGROUND: 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. METHODS: AD rats were induced by injecting ß-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. RESULTS: Morris 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. CONCLUSIONS: Our 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.

[Experimental study of inhibition of safflower injection on mesenteric microvascular motion in rabbits DI].

OBJECTIVE: To dynamically observe the effect of Safflower Injection (SI) on mesenteric microvascular motion in vivo in rabbits, and to explore the effect of nitric oxide (NO) in the process to further investigate the action mechanism of activating blood to remove stasis of SI. METHODS: Twenty healthy male albino rabbits were intraperitoneally injected with urethane for basic anesthesia and injected with alpha-chloralose via ear marginal venous to maintain anesthesia, spontaneously ventilated via tracheotomy tube, with the in-step record of breath and blood pressure. The vasomotion was induced by noradrenaline (NA) in vivo, then the changes of vasomotion after injecting SI and N(G)-monomethyl-L-arginine (L-NMMA, a NO synthase inhibitor) were measured respectively on a TV monitor using a TV camera mounted on the microscope, and the influence of L-NMMA on effect of SI was also observed. RESULTS: L-NMMA injection alone can inhibit the NA induced vasomotion in vasoconstriction state, while SI injection alone can inhibit it in vaso-dilation state. SI could abolish the effect of L-NMMA on vasomotion but L-NMMA did not influence the effect of SI on vasomotion. CONCLUSION SI can inhibit vasomotion in vaso-dilation status, but its mechanism is not mediated by endogenous NO.