Treatment For AD Rats With Small Molecular Bovine Acidic Neuropeptide And Its Mechanism

Background and PurposeAlzheimer's disease(AD), characterized clinically by progressive loss of memory and cognition, pathologically by senile plaques(SP), neurofibrillarytangles(NFT), and synapse loss, is an age-related neurodegenerative disorder. The primary pathogeny and cause of AD remains unknown. The morbidity of AD is high among the elderly. In developed countries AD has already been the fourth leading cause of death after heart disease, cancer and stroke for lack of effective early diagnostic and therapeutic methods. So it's very imP<0rtant and urgent to actively study AD.The nucleus basalis of Meynert (nbM) locates in the base of the forebrain. Almost all of neurons in nbM are cholinergic neuron. Neurofibers sending out from nbM project into hipP<0campus, cerebral cortex and other brain regions. Ibotenic acid (IBO) is a kind of NMDA receptor agonist with strong excitatory neurotoxin. It can damage the learning and memorial ability of the rat eternally and steadily. The ideal animal model can be made by injecting IBO into the nbM of the rat.Neuropeptides are some imPortant substances which have functions of neuronal signal transmission and regulation. They distribute widely in the central nervous system, and participate in many kinds of functional regulation. An Yuhui has isolated some small neuropeptides from bovine brains and found a new peptide: bovine acidic neuropeptide 1 (BANP-1). It is a small molecular peptide and has not antigenicity. Animal experiments have proved that it can increase amino acid of brain and affect the contents of cGMP of brain. In this study, the effects of BANP-1 on ADmice were observed by setting up AD mouse model, in which IBO was injected into the nbM of the rats. The curing mechanism of BANP-1 to AD rats was studied by analysis of some biochemical substances. The purP<0se of this research is to accumulate valuable data for researching pathogenesis of AD and to explore new medicine for treatment of AD. Materials and MethodsEighty-four healthy male SD rats (8-12weeks, 170-210g) were randomly divided into 7 groups and each group contained 12 rats. In the research, AD animal model is established by injecting IBO 1μl (5μ g) into rats brain to damage bilateral nbM in rats brain. I group was normal group; II group was AD animal model; III, IV, V, VI,VII group was AD animal model + orally normal saline, Naofukang 0.3g/kg ·d, BANP-1 15mg/ kg·d, BANP-1 30mg/ kg·d, BANP-1 60mg/ kg·d respectively. Normal control group and model group rats had not been treated. This process had lasted for 20 days, once every day, each time 2ml. After AD rats were treated with naofukang and different dosages of BANP-1, the learning and remembering ability was tested by Y-maze experiment and jumping table experiment at the same time. Then all rats were decapitated, blood was collected and serum was isolated. The brain was homogenized and centrifugalized to examine neurobiochemistrical assay .The experimental data were expressed by and analyzed by one-way analysis of variance (ANOVA). a =0.05 was the standard of test. Results1 .Comparing with normal control group: The learning and remembering abilityof model group decreased significantly (P<0.01) ; the total protein of brain of modelgroup decreased significantly (P<0.05) ; though the glutathione (GSH) of brain ofmodel group decreased, it had no significant differences (P>0.05); T-AOC andSOD of brain of model group decreased significantly (P<0.01), MDA of themincreased significantly (P<0.01) ; AChE of brain of model group decreasedsignificantly (P<0.01 ) ;Na+-K+-ATPase of brain of model group decreased.significantly (P<0.05) ,LD of brain of model group increased significantly(P<0.05 ),LDH of brain of model group decreased significantly (P<0.05 );NO andNOS of brain of model group increased significantly (P<0.01) ; The total protein, T-AOC and CAT of serum of odel group had no significant differences (P>0.05 ); . SOD of serum of model group decreased s...