2. Academic Validation
  3. A medicine and food homology formula prevents cognitive deficits by inhibiting neuroinflammation and oxidative stress via activating AEA-Trpv1-Nrf2 pathway

A medicine and food homology formula prevents cognitive deficits by inhibiting neuroinflammation and oxidative stress via activating AEA-Trpv1-Nrf2 pathway

  • Inflammopharmacology. 2024 Sep 21. doi: 10.1007/s10787-024-01570-4.
Ming-Jie Li 1 2,  Jing-Yi Xu 3,  Hua-Yue Zhang 1,  Min Guo 1,  Meng-Ning Lan 1,  Jie Kong 1,  Shi-Wei Liu 4,  Hua-Jun Zheng 5
Affiliations

Affiliations

  • 1 Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, 200237, China.
  • 2 College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • 3 School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, Shenyang, 117004, China.
  • 4 Shanghai Xizuo Biotechnology Co., Ltd, Shanghai, 201107, China.
  • 5 Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, 200237, China. zhenghj@chgc.sh.cn.
PMID: 39305407 DOI: 10.1007/s10787-024-01570-4
Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder frequently accompanied by neuroinflammation and oxidative stress. The medicine and food homology (MFH) has shown potential for treating neuroinflammation and oxidative stress. This study aimed to provide a safe and efficient therapy for AD based on MFH. In this study, we develop a MFH formula consisting of egg yolk oil, perilla seed oil, raphani seed oil, cinnamon oil, and noni puree (EPRCN). To evaluate the ameliorative effects of EPRCN on AD-related symptoms, a mouse model of AD was constructed using intraperitoneal injection of scopolamine in ICR mice. Experimental results demonstrated that EPRCN supplement restored behavioral deficits and suppressed neuroinflammation and oxidative stress in the hippocampus of scopolamine-induced mice. An in vitro study was then performed using induction of Aβ(25-35) in glial (BV-2 and SW-1783) and neuron (SH-SY5Y) cell lines to examine the improvement mechanism of EPRCN on cognitive deficits. Multi-omics and in vitro studies demonstrated that these changes were driven by the anandamide (AEA)-Trpv1-Nrf2 pathway, which was inhibited by AM404 (an AEA inhibitor), AMG9810 (a Trpv1 inhibitor), and BT (an Nrf2 inhibitor). Consequently, EPRCN is an effective therapy on preventing cognitive deficits in mouse models of AD. In contrast to donepezil, EPRCN exhibits a novel modes action for ameliorating neuroinflammation. The mechanism of EPRCN on preventing cognitive deficits is mediated by improving neuroinflammation and oxidative stress via activating the AEA-Trpv1-Nrf2 pathway.

Keywords

AEA–Trpv1–Nrf2 pathway; Alzheimer’s disease; Medicine and food homology; Neuroinflammation; Oxidative stress.

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