| Objective : To study the effects of ginsenoside Rga on neurodegeneration of hippocampal CA1 cells in Alzheimer'disease(AD) animal model and to investigate the possible pathological mechanisms of the effects.Methods: Incubated-A 3 1.40 and Ibotenic Acid were micro-injected into the left hippocampus CA1 region of the rats to establish a rat model with disorders of learing and memory . Different dosage of ginsenoside Rg2 were given respectively for treatmemt(contrasting with nimodipine).The performance of Y-maze task were studied in the rats for the changes of learing and memory abilities.The neuropathological changes were studied in haematoxylin-eosin(HE) and NISSLE staining,and expression of Bcl-2, Bax, C-fos in the hippocampi of injection side were observed in Immunohistochemistry assay to identify the morphological characters and density of neuronal apotosis in hippocampus with TUNEL .Results: The capabilities of learning and memory were defected significantly in rats treated with A P MO and IB A.The capabilities were improved significantly with the middle and high dosage of ginsenside Rg2 .The HE staining revealed that co-injection of A3 1.40 and IBA produced drastic loss of neurons .A number of glial cells infiltrated in the injection site. The degeneration of neurons was limited around the injection site in rat groups treated with ginsenside Rg2, and no obvious morphological changes were observed in the distant regions from the site. NISSLE staining showed that neuronal lost significantly in hippocampus CA1 region in model groups.In contrast to ginsenside Rg2 treated groups, ginsenside Rg2 could inhibit neuronal loss.TUNEL assay-possitive cells ,i.e. apoptotic cells, were frequently detected in whole hippocampus CA1 region in model group , and were observed only around injection site in ginsenoside Rg2 groups. The expression of Bcl-2 was dereased, that of Bax was increased in model group, and which were reversed in ginsenoside Rg2 treated groups. Ginsenside Rg2 could enhance expression of C-fos in brain of the rat, and the effects were dose-dependent.Conclusions: Neural toxity in vivo can be induced exactly by co-injection of coacervated-type A B MO and IBA in the hippocampus , which could be partlymodeled behavior and pathological characterization of AD. Impairment of learning and memory could be improved by ginsenoside Rg2 treatment in AD model rat ,which might be related to improved expression of C-fos and the expression of apotosis promoting gene Bax and inhibiting gene Bcl-2, therefore that decreased the number of apotosis cell induced by injected neurotoxicity drug ,and prevented the neurons from damage.
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