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Abstract <p>Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by abnormal amyloid-<i>β</i> protein (A<i>β</i>) deposition and tau protein hyperphosphorylation (p-tau), yet effective therapeutics remain scarce. Aloe emodin (AE) is a natural anthraquinone derivative that demonstrates neuroprotective effects. However, its specific therapeutic efficacy and functional mechanism are not fully elucidated. To address this, we investigated AE’s mechanism in AD treatment using a network pharmacology approach. This analysis revealed that 83 common targets shared by AE and AD, enriched in processes such as apoptosis and protein phosphorylation. Mitogen-activated protein kinase 14 (MAPK14, also known as p38) was identified as a key target. KEGG pathway analysis further confirmed that the key mechanism of AE in AD treatment was mediated by the MAPK signaling pathway. Subsequent molecular docking and dynamics simulations demonstrated that the AE-p38 complex exhibited strong binding affinity and high stability. Building on these predictions, in vitro studies confirmed that AE enhanced cell viability and modulated the MAPK pathway. Critically, p38-specific inhibition experiments demonstrated that AE alleviated A<i>β</i> accumulation and tau hyperphosphorylation through inhibiting p38. In conclusion, this study demonstrates that AE protects against A<i>β</i><sub>25–35</sub>-induced neurotoxicity in HT22 cells, primarily by inhibiting the p38 MAPK signaling pathway.</p> Graphical abstract <p></p>

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Aloe-emodin inhibits p38 MAPK pathway in Alzheimer’s disease treatment: a network pharmacology and experimental verification

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Zhaorong Ouyang,
  • Fei Liu,
  • Qingyang Lu,
  • Yuan Wang,
  • Nan Shao,
  • Houli Liu,
  • Biao Cai

摘要

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by abnormal amyloid-β protein (Aβ) deposition and tau protein hyperphosphorylation (p-tau), yet effective therapeutics remain scarce. Aloe emodin (AE) is a natural anthraquinone derivative that demonstrates neuroprotective effects. However, its specific therapeutic efficacy and functional mechanism are not fully elucidated. To address this, we investigated AE’s mechanism in AD treatment using a network pharmacology approach. This analysis revealed that 83 common targets shared by AE and AD, enriched in processes such as apoptosis and protein phosphorylation. Mitogen-activated protein kinase 14 (MAPK14, also known as p38) was identified as a key target. KEGG pathway analysis further confirmed that the key mechanism of AE in AD treatment was mediated by the MAPK signaling pathway. Subsequent molecular docking and dynamics simulations demonstrated that the AE-p38 complex exhibited strong binding affinity and high stability. Building on these predictions, in vitro studies confirmed that AE enhanced cell viability and modulated the MAPK pathway. Critically, p38-specific inhibition experiments demonstrated that AE alleviated Aβ accumulation and tau hyperphosphorylation through inhibiting p38. In conclusion, this study demonstrates that AE protects against Aβ25–35-induced neurotoxicity in HT22 cells, primarily by inhibiting the p38 MAPK signaling pathway.

Graphical abstract