西红花乙酸乙酯部位的神经保护活性及作用机制研究OA

Based on the concept of the homology of medicine and food,this study aimed to investigate the neuroprotective effects and underlying mechanisms of the saffron(Crocus sativus L.)ethyl acetate fraction(SEA)against Alzheimer's disease(AD).LC-MS/MS was used to identify the absorbed blood components of SEA,and its core anti-AD pathways were predicted using network pharmacology.An Aβ25-35-induced PC12 cell injury model was established to evaluate the effects of SEA on cell viability,morphology,apoptosis,and oxidative stress-related indicators,including glutathione peroxidase(GSH-Px),superoxide dismutase(SOD),and catalase(CAT)activities.Furthermore,untargeted metabolomics was applied to identify key pathways involved in differential metabolites.The results showed that a total of 27 prototype components were identified via LC-MS/MS,from which 37 candidate components with favorable oral absorption and drug-like properties were screened using ADMET-AI.Network pharmacology analysis revealed that the therapeutic core of SEA was highly correlated with the"oxidative stress response-apoptosis regulation"pathway.In vitro,SEA treatment significantly increased the viability of Aβ25-35-damaged PC12 cells,improved cell morphology,enhanced GSH-Px,SOD,and CAT activities,and decreased the apoptosis rate across all dose groups.Metabolomics analysis confirmed that the differential metabolites were primarily involved in 8 metabolic pathways,including the biosynthesis of unsaturated fatty acids and pyrimidine metabolism.In conclusion,the SEA exhibited significant neuroprotective activity.Its mechanism of action was likely mediated through the regulation of oxidative stress,inhibition of apoptosis,and modulation of multiple metabolic pathways.