论文部分内容阅读
目的通过建立血管性痴呆(VD)大鼠模型,观察松果菊苷(ECH)对VD大鼠学习记忆及海马组织脑源性神经营养因子(BDNF)、酪氨酸激酶B(TrkB)表达的影响。方法取SD大鼠随机分为假手术组、模型组和ECH组(30 mg·kg~(-1)),每组30只。采用永久性结扎双侧颈总动脉建立大鼠VD模型,ECH组给予ECH治疗4周,采用Morris水迷宫检测学习记忆能力,处死大鼠取脑,分离皮层与海马组织,HE染色观察脑组织神经元损伤。RT-PCR法测定海马组织BDNF、TrkB mRNA表达,Western blot法检测BDNF、TrkB、AKT蛋白表达水平,免疫组化法测定N-甲基-D-天冬氨酸受体(NMDAR)蛋白的表达。结果与假手术组比较,模型组大鼠逃避潜伏期延长,穿越平台次数降低(P<0.05),脑组织皮质及海马组织神经元损伤明显,海马组织BDNF、TrkB mRNA表达及BDNF、TrkB、AKT、NMDAR蛋白表达低于假手术组(P<0.05);与模型组比较,ECH组大鼠逃避潜伏期缩短,穿越平台次数增加(P<0.05),脑组织皮质及海马组织神经元损伤明显改善,海马组织BDNF、TrkB的mRNA表达及BDNF、TrkB、AKT、NMDAR蛋白表达明显高于模型组(P<0.05)。结论松果菊苷可能通过上调VD大鼠海马区BDNF、TrkB、AKT、NMDAR表达,减轻VD大鼠神经元缺血损伤,改善学习记忆能力。
OBJECTIVE: To establish a rat model of vascular dementia (VD) and observe the effects of echinacoside (ECH) on the learning and memory and the expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) in hippocampus of VD rats. influences. Methods SD rats were randomly divided into sham operation group, model group and ECH group (30 mg · kg -1), with 30 rats in each group. The rat model of VD was established by permanent ligation of bilateral common carotid arteries. ECH group was treated with ECH for 4 weeks. Morris water maze was used to detect the learning and memory abilities. Rats were sacrificed and cortex and hippocampus were isolated. HE staining was used to observe the changes of nerve Yuan injury. The expression of BDNF and TrkB mRNA in hippocampus was detected by RT-PCR, the expression of BDNF, TrkB and AKT were detected by Western blot and the expression of N-methyl-D-aspartate receptor (NMDAR) protein by immunohistochemistry . Results Compared with the sham operation group, the escape latency and the number of passing through the platform in the model group were significantly decreased (P <0.05). The neurons in the cortex and hippocampus of the model group were significantly damaged. The expressions of BDNF, TrkB mRNA and the expressions of BDNF, TrkB, AKT, (P <0.05). Compared with the model group, the escape latency and the number of passing through the platform of ECH group were significantly increased (P <0.05), the damage of neurons in cerebral cortex and hippocampus was significantly improved, and the hippocampus The mRNA expression of BDNF and TrkB and the protein expressions of BDNF, TrkB, AKT and NMDAR were significantly higher in model group than those in model group (P <0.05). Conclusion Echinacoside may decrease the neuronal ischemic injury and improve learning and memory in VD rats by up-regulating the expression of BDNF, TrkB, AKT and NMDAR in hippocampus of VD rats.