摘要
目的研究灵芝多糖(GLP)对Aβ25-35诱导阿尔茨海默病模型大鼠脑组织的影响。方法采用双侧海马内一次性注射β-淀粉样多肽25-35片段(Aβ25-35)制作大鼠AD模型,再连续7天腹腔注射GLP,随后进行行为学测定,采用HE染色、透射电镜及免疫组织化学等方法检测海马神经元的结构变化及反应性星形胶质细胞活化程度的影响。结果海马内注射Aβ25-35后海马细胞增生、聚集,核边聚、碎裂,电镜观察显示,锥体细胞胞浆水肿,内质网池扩张,星形胶质细胞增生肥大,GLP组病变显著减轻,超微结构尚属正常,海马星形胶质细胞较AD组显著减少。结论灵芝多糖对Aβ25-35诱导阿尔茨海默病模型大鼠脑组织内海马退行性变神经元有一定的保护作用,并能降低脑组织内的神经炎症反应。
Objective To study the influence of Ganoderma Lucidum Polysaccharide on the brain tissue of rat model of Alzheimer＇s disease induced by β-Amyloid peptide frag.ment 25-35. Methods Microinjection of Aβ25-35 into the hippocampus induced learning and memory dysfunction in rats. 7 days after intra-abdominal injection of Ganoderma Lucidum Polysaccharide, the rats were placed into the Morris maze to test intelligence. Then HE histochemistry, transmission electron microscopy and GFAP staining were employed to study the influence of Ganoderma Lucidum Polysaccharide on the brain of the rat model. Results The neurons in the hippocampus of rats injected with Aβ25-35 showed such ultrastructural pathological changes as cell increase, endoplasmic reticulum dilatation, chromatin agglomeration, and astrocyte hypertrophy. In the GLP group the pathological changes were alleriated. The ultrastructure was almost normal, and the number of astrocytes was significantly decreased as compared with that of the Alzheimer＇s disease group. Conclusion Ganoderma Lucidum Polysaccharide provides marked neural protection, significantly decreasing the neuritis in the brain of the rat model of Alzheimer＇s disease induced by β-Amyloid peptide fragment 25-35.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2006年第4期447-451,共5页
Chinese Journal of Histochemistry and Cytochemistry
基金
湖北省自然科学基金资助项目(2003ABA170)
