Effects Of Tenuigenin On Learning And Memory And Expression Of Nicotinic Acetylcholine Receptor Subunit Alpha-7 In Hippocampus Of AD Rats

Alzheimer’s disease (AD) has become a more and more hot issue in modern society with theacceleration of population senescence in the world.Alzheimer’s disease (AD) is the most common cause of dementia among older people. Therisk goes up as you get older,The term ’dementia’ describes a set of symptoms which can includea decline in cognitive function or mental ability,thinking,reasoning and remembering.Alzheimer’s is a progressive disease, Currently there is no cure for Alzheimer’s disease. However,drug treatments can temporarily alleviate some symptoms or slow down their progression insome people. Many individuals with Alzheimer’s have been shown to have a shortage of thechemical acetylcholine in their brains.The decreased activity of cholinergic system is Currently recognized,which is one of important reasons for the cause of AD. The expression of nicotinicacetylcholine receptor (nicotinic acetylcholine receptors, nAChRs) in the brain of AD isdecreased,which is a common phenomenon.Experiments show that compared with the controlgroup,the memory of the rats which were the lack of nAChRα7 subunits was decreased in theMorris water maze test.Tenuifolin(TEN) is a crude extract of Polygala tenuifolia Willd.which is commonly used intraditional Chinese herbal medicine for nootropic.Previous studies have shown that tenuigenin,can improve learning and memory ability. However, the mechanism underlying this effect isunknown.The impact of TEN on the expression of Nicotinic Acetylcholine Receptor subunit alpha-7in hippocampus region of Alzheimer’s disease model has not been reported.In this study，the model of Alzheimer’s disease was made by orientally injecting ibotenicacid into Meynert basal nuclei of aging rat induced by D-gal. Morris maze test was used toevaluate the learning and memory of each rat, Immunohistochemistry was performed to estimatethe changes of the expression of Nicotinic Acetylcholine Receptor subunit alpha-7 inhippocampus region of rats.PartⅠEffects of Tenuigenin on Learning and Memory Of AD RatsObjective: To observe the effects of TEN on learning and memory of AD rats caused byD-gal and IBO, and to prove whether the effects are dose-dependent.Methods: 32 male Wistar rats were randomized into control group, model group, high-dosegroup and low-dose group. The model of Alzheimer’s disease was made by orientally injectingibotenic acid into Meynert basal nuclei of aging rat induced by D-gal Morris maze test was usedto evaluate the learning and memory of each rat.Results:①In the five days of the place navigation test, the escape latency of each rats weregradually decreased;Compared with control group,the average escape latency of the high doseTEN group were significantly prolonged(P<0.05).Compared with model group,the averageescape latency of the high and low dose TEN group were significantlyshortened(P<0.05);Compared with control group,the average escape latency of the model groupwere significantly prolonged(P<0.05).②Compared with control group, the times of passingplatform was significantly decreased, (P<0.05）and the time of staying at platform quad wassignificantly shortened（P<0.05）in model group; Compared with model group, the times ofpassing platform were significantly increased（P<0.05）and the time of staying at platform quadwere significantly prolonged（P<0.05）, in both high dose group and low dose group; Furthermore, Compared with low dose group,the time of staying at platform quad and the timesof passing platform was significantly increased（P<0.05）in high dose group.Conclusion: This data suggests that TEN can improve learning and memory ability of ADrats potentially dose-dependently.PartⅡEffects of Tenuigenin on the expression of Nicotinic AcetylcholineReceptor subunit alpha-7 in hippocampus Of AD RatsObjective: To observe the effects of TEN on the expression of Nicotinic AcetylcholineReceptor subunit alpha-7 in hippocampus CA1 region Of AD Rats caused by D-gal and IBO.Toinvestigate the mechanism underlying the effects of TEN on learning and memory; and to provewhether the effects are dose-dependent.Methods: The group assigned as PartⅠ. Perfusion,solidification,takeing the brain,slicing ofspecimen and immunohistochemistry（SABC）were performed to estimate the changes of theexpression of Nicotinic Acetylcholine Receptor subunit alpha-7 in hippocampus CA1 region ofratsAfter Morris maze test.Results: Compared with control group, the expression of Nicotinic AcetylcholineReceptor subunit alpha-7 in hippocampus CA1 region of model group obviouslydeclined(P<0.05). The expression of Nicotinic Acetylcholine Receptor subunit alpha-7 inhippocampus CA1 region in high and low dose Tenuigenin treatment group decreasedsignificantly(P<0.05)compared with the model group. Compared with the low dose Tenuigenintreatment group, the expression of Nicotinic Acetylcholine Receptor subunit alpha-7 inhippocampus CA1 region in high dose Tenuigenin treatment group increasedsignificantly(P<0.05).Conclusion: This data suggests that TEN can potentially dose-dependently increase theexpression of Nicotinic Acetylcholine Receptor subunit alpha-7 in hippocampus CA1 region ofAlzheimer’s disease model rats, which may partly explain the beneficial effects of TENon learning and memory and cognitive function.