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Neurons’ Apoptosis of AD Rats and Protection of Traditional Medicine

Author: QiLi
Tutor: MaDiHui
School: Jilin University
Course: Department of Neurology
Keywords: Alzheimer's disease Cytochrome C Bcl-2 Aβ
CLC: R749.16
Type: Master's thesis
Year: 2006
Downloads: 113
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Abstract

Clinical manifestation of Alzheimer’s disease (AD) is progressivedecreased ability of learning and memory, up to lose. The characters ofpathology are atrophy of cortex, hippocampus and white matte of brain.primary degeneration of neurons especially cholinergic neurons. Theneuropat-hology of AD is complex, characterized by senile plaque andneurofilament tangle. The other features include vacuolar degenerationof neuron, neuronal loss, abnormal axonal and synaptic changes andthe reaction of astrocyte and microglia. Neuronal loss may be theresult of neuronal apoptosis. Experiments have approved: Neuronalloss may be the result of neuronal apoptosis. Hippocampus is oftendamaged. Bcl-2 is a protooncogene, separated from lymphocyte of human,Its function is reduce apoptosis. It is a effective restrain apoptosis genein nerve centre system, It advance regeneration of nerve cells. The highexpression of Bcl-2 in hippocampus relating to learning and memory.Presently, Bcl-2 do not check apoptosis lonely, together with help of itsfamily members. The findings of study: Bax is a skeleton crew of itsfamily members. Bax will hasten apoptosis. The polymer that consistsof Bcl-2 and Bax, which is necessary to counteract apoptosis. Whencell is stimulated, living or dead rest with the rate of Bcl-2/Bax, If therate is high cell will be living. Otherwise, cell will be die. Thespecifiable mechanism that we do not know until today.Mitochondria act a key role in apoptosis, its function is to releaseof caspase and activate cytochrome c. Cytochrome c frommitochondria into cytosol is sufficient to elicit apoptosis. As we nowknow, Cyto-C function in apoptosis. It is a basic component ofrespiratory chain. It is a soluble protein on the plasma membrane ofmitochondria. It is an important step of apoptosis that cytochrome cfrom mitochondria into cytosol. Such as apoptosis models: Fas, UV,staur osporin, VP16. When cytochrome c was find in cytosol, will beinteraction with others elements. It will activate casepases to induceapoptosis. Based on the hypothesis of AD, most of drugs are designedto elevate Ach content in the central nervous system and confrontapoptosis to improve memory and cognition. Some drugs are nutrientsof nerve such as traditional medicine has been proved to be helpful toimprove the behavior of AD sufferer. Our aims are to discuss neurons’apoptosis of AD rats and protection of traditional medicine. In the end,traditional medicine can control apoptosis and decrease the apoptoticneuron have been proved.In this experiment the model of AD was made by injection ofbeta-amyloid peptide (Aβ) in hippocampus. Changes of memory andstudy of AD rats were observed using water labyrinth. The changesthat CA1 section were observed by through optical microscope andtransmitssion electron microscope. Using the method of immunohisto-chemistry to test expression of Bcl-2 and Cyto-C. The results are asfollows:Solitary shrunken cells existed in the hippocampus, the chromatinof these round or ellipse cells aggregated to form royal blue compactplaque, the plasma also shrunk and was increased eosinophilic. Thenuclear membrane disappeared, but the cellular membrane was intact.Observed under electron microscopy, pyknosis could be seen in theneuron, other apopto-tic changes included unclear nuclear membrane,irregular morphologic and dissymmetric nucleus, border-aggregatedchromatin, compact and densely stained nucleus and plasma matrix.After the operation, at the first week, the second week and the firstmonth. Using water labyrinth to test changes of memory that all kindsof groups, including normal group, pseudo-operation group, traditionalmedicine group, Dukex group and AD group. Compared with ADgroup, traditional medicine group and Dukex group latency wassignificantly shorter. But compared with normal group, the latency wassignificantly longer. So we made a conclu-sion that traditionalmedicine could obviously improve the cognitive and behavior scoresof AD rats.We have test the expression of Bcl-2 and Cyto-C by using themethod of immunohistochemistry. It was founded that the rate of Bcl-2expression in normal group and pseudo-operation group were lowerthan others. Then the rate of expression in traditional medicine groupand Dukex group were higher than AD group. The level of expressionof Cyto-C in operated groups were higher than in others groups.Compared with treatment group, the level of expression In AD groupwas significantly increased. The result suggest: after apoptosis, the rateof expression of Bcl-2 and Cyto-C were increased. Cyto-C inducedhigh level of apoptosis, But the effect of Bcl-2 was opposition. Inconclusion, traditional medicine make use of theory that increased thecontent of Bcl-2 and decreased the content of Cyto-C to controlapoptosis.Traditional medicine was proved to control apoptosis anddecrease the apoptotic neuron. This effect was confirmed thattraditional medicine could also improve the ability of learning andmemory of AD rats.

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