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目的研究乙酰葛根素对β-淀粉样肽1-42(Aβ1-42)海马立体定位注射所致阿尔茨海默病(AD)模型大鼠的药物作用和对炎症因子蛋白激酶C-δ(PKC-δ)、白细胞介素-6(IL-6)表达的影响。方法将40只Wistar大鼠随机分为对照组、模型组、乙酰葛根素低、高剂量组。用Aβ1-42双侧海马注射制备AD大鼠模型,Morris水迷宫测定不同时期各组大鼠的学习记忆能力,ELISA测定血清IL-6含量的变化,Western blotting测定PKC-δ表达的变化。结果模型大鼠应用Aβ1-42注射14d后,Morris水迷宫逃避潜伏期与术前及对照组比较显著延长,穿越平台次数显著减少(P<0.01);应用乙酰葛根素10d后,血清中IL-6的表达量模型组显著高于对照组、乙酰葛根素低、高剂量组(P<0.01);海马匀浆中PKC-δ的表达量模型组显著高于对照组、乙酰葛根素低、高剂量组,乙酰葛根素低、高剂量组表达仍高于对照组(P<0.05)。结论乙酰葛根素能显著改善阿尔茨海默病模型大鼠的学习记忆能力,对阿尔茨海默病有显著的预防和保护作用,机制可能与调控PKC-δ/Caspase通路,抑制β-淀粉样肽的神经毒性,降低PKC-δ、IL-6的表达,从而发挥抗痴呆的作用。
Objective To investigate the pharmacological effects of acetylpuerarin on Alzheimer’s disease (AD) model rats induced by β-amyloid peptide 1-42 (Aβ1-42) hippocampal stereotactic injection and its effect on the expression of inflammatory cytokine protein kinase C-δ -δ), interleukin-6 (IL-6) expression. Methods Forty Wistar rats were randomly divided into control group, model group, low and high dose of acetylpuerarin. AD rats were injected with Aβ1-42 bilateral hippocampus. Morris water maze was used to measure the learning and memory abilities of rats in different periods. Serum IL-6 levels were measured by ELISA. The expression of PKC-δ was detected by Western blotting. Results After 14 days of Aβ1-42 injection, the escape latency of Morris water maze was significantly prolonged and the number of traversing platform significantly decreased (P <0.01). After 10 days of application of acetyl puerarin, the level of IL-6 (P <0.01). The expression of PKC-δ in hippocampal homogenate model group was significantly higher than that of the control group, with low and high doses of acetyl puerarin Group, the expression of acetyl puerarin low and high dose group is still higher than the control group (P <0.05). Conclusions Acetylpuerarin can significantly improve the learning and memory ability of Alzheimer’s disease model rats, and has a significant preventive and protective effect on Alzheimer’s disease. The mechanism may be related to the regulation of PKC-δ / Caspase pathway and the inhibition of β-amyloid Peptide neurotoxicity, reduce the expression of PKC-δ, IL-6, thus play the role of anti-dementia.