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目的:运用超高效液相色谱质谱(UPLC-MS)技术研究黑水缬草提取物对Aβ_(25-35)诱导所致阿尔茨海默病(AD)模型小鼠的干预机制,为AD治疗提供新的思路。方法:将实验小鼠随机分为3组:对照组、AD模型组和治疗组,运用免疫组化实验观察AD小鼠脑部组织病理学改变,运用UPLC-MS技术研究黑水缬草提取物对AD模型小鼠生物标记物的调控作用。结果:对照组小鼠海马区细胞排列整齐且形态正常。AD模型组小鼠海马区可见到大量淀粉样斑块。治疗组小鼠海马区淀粉样斑块数量减少,细胞趋于正常。通过对实验小鼠血浆代谢组学进行分析,确定了色氨酸、组氨酸、溶血磷脂酰胆碱(LPC)C22∶6、LPC C18∶2、LPC C16∶0(m/z 496.2)、LPC C16∶0(m/z 991.6)、二氢神经鞘氨醇(DHS)、C16 DHS、C20 DHS、十八碳4-羟双氢(神经)鞘氨醇(C18PHS)、C20 PHS 11种AD血浆生物标记物,通过比较发现,AD模型组小鼠血浆中11种标记物含量较对照组均显著降低(P<0.01),而治疗组小鼠血浆中11种生物标记物含量较AD模型组均明显上升(P<0.05,P<0.01)。结论:黑水缬草提取物可通过干预AD小鼠体内氨基酸、磷脂和鞘脂等相关代谢通路而缓解小鼠海马区淀粉样斑块沉积,从而起到治疗AD作用。
OBJECTIVE: To investigate the mechanism of Valerian extract on the Alzheimer’s (AD) model mice induced by Aβ_ (25-35) by ultra performance liquid chromatography-mass spectrometry (UPLC-MS) Provide new ideas. Methods: The experimental mice were randomly divided into three groups: control group, AD model group and treatment group. Immunohistochemistry was used to observe the histopathological changes of brain in AD mice. UPLC-MS was used to study the effects of Valerian extract Modulation of Biomarkers in AD Model Mice. Results: The cells in the hippocampus of the control group were arranged neatly and were normal in morphology. A large number of amyloid plaques were found in hippocampus of AD model mice. The number of amyloid plaques in the hippocampus of mice in the treatment group decreased and the cells tended to be normal. By analyzing the plasma metabolomics of experimental mice, tryptophan, histidine, lysophosphatidylcholine (LPC) C22: 6, LPC C18: 2, LPC C16:0 (m / z 496.2) LPC C16: 0 (m / z 991.6), dihydrosphingosine (DHS), C16 DHS, C20 DHS, octadecyl 4- Compared with the control group, the content of 11 biomarkers in the plasma of the AD model group was significantly lower than that of the control group (P <0.01), while the content of 11 biomarkers in the plasma of the treatment group was significantly higher than that of the AD model group Were significantly increased (P <0.05, P <0.01). Conclusion: Valeriana officinalis L. extract can relieve the amyloid plaque deposition in the hippocampus of mice by interfering with the related metabolic pathways of amino acids, phospholipids and sphingolipids in AD mice and thus play an active role in the treatment of AD.