Authors
Fang Huang, Mingxing Guo, Yiran Yang, Zhizhong Wang
Published in
Open medicine (Warsaw, Poland). Volume 21. Issue 1. Pages 20261473. Epub Jul 07, 2026.
Abstract
To study the role and underlying mechanism of aloe emodin, a natural anthraquinone compound known for antioxidant, and anti-inflammatory activities, in Alzheimer's disease (AD).
Aβ1-42-induced injury model was established using SH-SY5Y cells. A combination of CCK-8 assay, flow cytometry, ELISA, ROS fluorescence probe, RT-qPCR, and western blot assay was employed to systematically evaluate the effects of aloe emodin on cell viability, apoptosis, inflammation, and oxidative stress. Potential molecular targets were identified through bioinformatics analysis. The regulatory role of PPM1K in aloe emodin-mediated neuroprotection was further validated using PPM1K overexpression experiments.
Bioinformatics analysis revealed that PPM1K is significantly upregulated in AD and showed predicted in silico binding with aloe emodin. Aloe emodin markedly improved the viability of Aβ1-42-treated SH-SY5Y cells, suppressed apoptosis, reduced the release of pro-inflammatory cytokines, and attenuated ROS generation, accompanied by the downregulation of PPM1K expression. In contrast, overexpression of PPM1K significantly weakened the neuroprotective effects of aloe emodin, as evidenced by decreased cell viability and increased levels of apoptosis and oxidative stress.
Aloe emodin alleviates Aβ1-42-induced neuronal injury by targeting and downregulating PPM1K expression, suggesting that PPM1K is a critical mediator of the neuroprotective effects of aloe emodin.
PMID:
42416144
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.
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