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Unintegrated Approach to Uplc-Q-Tof-Ms-Based Analysis of Plasma Components and Metabolomics Profiling in Different Processed Products of Polygonatum Cyrtonema Hua. For the Treatment of Aβ25-35-Induced Alzheimer's Disease in Rat Plasma

仿形(计算机编程) 代谢组学 色谱法 化学 计算生物学 计算机科学 生物 操作系统
作者
Na Zhu,Lin‐Chun Wan,Xudong Zhu,Yi-Sheng Yang,Feixia Yan,Peng Zhang,Liping Huang,Yi Wu
标识
DOI:10.2139/ssrn.4707640
摘要

Polygonatum cyrtonema hua. (PCH) is a famous traditional homologous medicine and food used for over 1700 years in China and East Asia for pre-treating age-associated diseases in clinical settings. For the first time, we investigated the therapeutic effects of three distinct PCH-processed products in treating Alzheimer's disease (AD). Four types of pharmacodynamic evaluations, namely the Openfield test, the MWM, Aβ1-42, and p-Tau404 were used to assess the impact of the processed agents on rats with AD. Additionally, a plasma metabolomics analysis employing non-targeted ultra-performance liquid chromatography quadrupole-time-of-flight hybrid mass spectrometry (UPLC-Q-TOF-MS) technology, coupled with biosignature analysisto to investigate the role of different PCH processed products on the pathogenesis process in rats with AD. Results revealed that different processed products exhibited certain effects on improving the behavior and hippocampal pathology of rats with AD. Using Simca-p 14.0 for PCA and OPLS-DA analysis, combined with the HMDB database, identified 24 potential biomarkers displaying significant changes and highlighted four aberrant metabolic pathways, including sulfur metabolism, glycerophospholipid metabolism, purine metabolism, and steroid hormone biosynthesis. Significant alterations in FC, biological function, and three metabolites (i.e., LysoPC (18:3 (9Z,12Z,15Z) / 0:0), LysoPC (16:1 (9Z) / 0:0), LysoPC (16:1 (9Z) / 0:0) were observed between the the model and blank groups. Treatment with different PCH-processed products led to different levels of regression, suggesting their potential as diagnostic biomarkers for AD. Sulfur metabolism and lipid metabolism emerged as key pathways for intervening in the pathogenesis of AD. This metabolomics analysis, utilizing UPLC-Q-TOF-MS, provides insights into the role of different PCH-processed products in intervening in the progression of AD. These findings deepen our understanding of the metabolic processes associated with AD and offer insights into the therapeutic mechanism of different PCH-processed products in rats with AD.
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