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目的:观察CCL4-CCR5轴对AD典型病变的影响及银杏叶提取物EGB761的干预作用。方法:选取8月龄SAMP8小鼠为痴呆模型,以灌胃的方式进行EGB761干预4周;并以同龄SAMR1小鼠为对照组,给予等量生理盐水灌胃。干预结束后,内眦取血并迅速取出脑组织,左侧脑组织行福尔马林固定,右侧脑组织分离出皮质及海马进行冻存。酶联免疫吸附法检测血浆Aβ40及Aβ42水平;免疫组织化学染色评估脑组织Aβ沉积情况;酶联免疫吸附法观察脑组织CCL4的表达并采用Western blotting法检测CCR5的表达。结果:与对照组相比,SAMP8小鼠血浆Aβ40及Aβ42水平升高(P<0.01),脑Aβ沉积加重;脑组织CCL4表达水平增高(P<0.01),CCR5表达也相应增高;EGB761能有效降低血浆Aβ40及Aβ42水平(P<0.01;P<0.05),减少Aβ沉积;并能抑制CCL4及CCR5的表达。结论:EGB761能有效缓解AD典型病变,可能与调控CCL4-CCR5轴影响神经炎症反应有关。
OBJECTIVE: To observe the effects of CCL4-CCR5 axis on the typical pathological changes of AD and the effect of GGB extract EGB761. Methods: Eight-month-old SAMP8 mice were selected as dementia model and intragastrically administered with EGB761 for 4 weeks. The same age SAMR1 mice were used as the control group, and normal saline was given intragastrically. After the intervention, blood was taken from the infrarenal vein and the brain tissue was quickly removed. The left brain tissue was fixed with formalin, and the cortex and hippocampus were isolated from the right brain tissue for cryopreservation. The levels of Aβ40 and Aβ42 in plasma were detected by enzyme-linked immunosorbent assay (ELISA), Aβ deposition in brain tissue was assessed by immunohistochemical staining, CCL4 expression in brain tissue was detected by enzyme-linked immunosorbent assay, and the expression of CCR5 was detected by Western blotting. Results: Compared with the control group, the levels of Aβ40 and Aβ42 in SAMP8 mice increased (P <0.01), the deposition of Aβ increased, the expression of CCL4 increased (P <0.01) and the expression of CCR5 increased Reduce plasma Aβ40 and Aβ42 levels (P <0.01; P <0.05), reduce Aβ deposition; and can inhibit CCL4 and CCR5 expression. Conclusion: EGB761 can effectively alleviate the typical pathological changes of AD, which may be related to the regulation of CCL4-CCR5 axis affecting neuroinflammation.