Dl-3 n-butylphthalide protects against the permeability changes of blood brain barrier by influencing tight junctions in Alzheimer ’ s disease

Alzheimer’s disease (AD) is a leading cause of morbidity among old people. Dl-3n-butylphthalide (NBP) is a novel agent and has a potential role on angiogenic activity and a good curative effect against cerebral ischemia. However, the molecular mechanism remains unclear. In order to explore the effect of NBP on the incidence and development of AD, we selected Male Wistar rats for study and separated them into 3 groups: NBP group (rats were intraperitoneal injected with NBP after permanent bilateral occlusion of the common carotid arteries), control group (rats underwent the same aforementioned protocol except for permanent bilateral occlusion of the common carotid arteries and NBP injection) and 2-VO group (rats underwent permanent bilateral occlusion of the common carotid arteries). The MWM task was performed to explore the potentiation of NBP on the cognitive and memory function of rats with AD. Rat cortex and hippocampus tissues were isolated. Immunohistochemistry and western blotting assays were used to determine the protein expression of APP, Aβ, VEGF and TJ claudin-5. Result showed the protein expression of VEGF and TJ claudin-5 decreased significantly in 2-VO group, while the expression of Aβ increased. However, Aβ expression decreased, and VEGF and TJ claudin-5 expression increased in NBP group compared with those in 2-VO group. Our results indicated NBP could affect the process of AD by influencing the tight junctions (TJs) of blood brain barrier (BBB).