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该文通过侧脑室注射Aβ_(1-42)联合2-VO建立AD大鼠模型,探究β-细辛醚对该模型学习记忆障碍的保护作用,并初步探讨其作用机制。将105只大鼠随机分为7组,分别为假手术组、AD模型组、β-细辛醚低、中、高剂量组(10,20,30 mg·kg~(-1))、多奈哌齐组(0.75 mg·kg~(-1))和银杏叶提取物组(24 mg·kg~(-1)),不同药物给药4周后检测大鼠学习记忆能力、局部脑血流量变化、海马CA1区病理改变、皮质HIF-1α水平及血清CAT,SOD和MDA水平。结果显示,侧脑室注射Aβ_(1-42)联合2-VO导致大鼠学习记忆障碍,局部脑血流量降低,CA1区神经元排列紊乱、出现大量空泡、淀粉样沉淀增多,皮质HIF-1α阳性细胞数显著增加,血清CAT和SOD显著下降,MDA显著上升。给予20,30 mg·kg~(-1)β-细辛醚后,上述症状均得到显著改善。结果表明,β-细辛醚能够缓解Aβ_(1-42)联合2-VO建立AD大鼠模型的症状,其作用机制可能是β-细辛醚通过提高机体抗氧化能力,降低体内的活性氧类物质,从而降低HIF-1α水平,减轻了过氧化物及HIF-1α对神经细胞的损伤,最终达到缓解AD的目的。
In this study, AD rat model was established by intracerebroventricular injection of Aβ 1-42 combined with 2-VO to explore the protective effect of β-asarone on learning and memory impairment in this model and its possible mechanism. 105 rats were randomly divided into 7 groups: sham operation group, AD model group, β-asarone low, medium and high dose groups (10, 20 and 30 mg · kg -1), donepezil (0.75 mg · kg -1) and Ginkgo biloba extract (24 mg · kg -1). After 4 weeks of administration, the learning and memory abilities, changes of local cerebral blood flow, Hippocampal CA1 area pathological changes, cortical HIF-1α levels and serum levels of CAT, SOD and MDA. The results showed that intracerebroventricular injection of Aβ 1-42 combined with 2-VO resulted in impaired learning and memory impairment, decreased local cerebral blood flow, disordered neurons in CA1 area, massive vacuoles, increased amyloid deposition, cortical HIF-1α The number of positive cells increased significantly, serum CAT and SOD decreased significantly, MDA increased significantly. After the administration of 20, 30 mg · kg -1 β-asarone, the above symptoms were significantly improved. The results showed that β-asarone could relieve the symptoms of AD rat model induced by Aβ 1-42 combined with 2-VO. The mechanism may be that β-asarone can reduce the body’s reactive oxygen species Class substances, thereby reducing the level of HIF-1α, reducing the peroxide and HIF-1α damage to nerve cells, and ultimately achieve the purpose of alleviating AD.