药食同源配方通过激活 AEA-Trpv1-Nrf2 通路抑制神经炎症和氧化应激，从而预防认知缺陷。

IF 4.6 2区医学 Q2 IMMUNOLOGY

Inflammopharmacology Pub Date : 2024-12-01 Epub Date: 2024-09-21 DOI:10.1007/s10787-024-01570-4

Ming-Jie Li, Jing-Yi Xu, Hua-Yue Zhang, Min Guo, Meng-Ning Lan, Jie Kong, Shi-Wei Liu, Hua-Jun Zheng

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引用次数: 0

摘要

阿尔茨海默病（AD）是一种神经退行性疾病，常伴有神经炎症和氧化应激。药食同源（MFH）已显示出治疗神经炎症和氧化应激的潜力。本研究旨在提供一种基于 MFH 的安全高效的 AD 治疗方法。在这项研究中，我们开发了一种由蛋黄油、紫苏籽油、鸦胆子油、肉桂油和诺丽果泥组成的药食同源配方（EPRCN）。为了评估EPRCN对AD相关症状的改善作用，我们在ICR小鼠腹腔注射东莨菪碱，构建了AD小鼠模型。实验结果表明，在东莨菪碱诱导的小鼠海马中，补充 EPRCN 可恢复行为缺陷，抑制神经炎症和氧化应激。随后，研究人员利用诱导神经胶质细胞系（BV-2和SW-1783）和神经元细胞系（SH-SY5Y）中的Aβ（25-35）进行了体外研究，以探讨EPRCN改善认知障碍的机制。多组学和体外研究表明，这些变化是由anandamide（AEA）-Trpv1-Nrf2通路驱动的，AM404（一种AEA抑制剂）、AMG9810（一种Trpv1抑制剂）和BT（一种Nrf2抑制剂）抑制了这一通路。因此，EPRCN 是一种有效的治疗方法，可防止小鼠 AD 模型出现认知障碍。与多奈哌齐相比，EPRCN在改善神经炎症方面表现出一种新的作用模式。EPRCN预防认知障碍的机制是通过激活AEA-Trpv1-Nrf2通路来改善神经炎症和氧化应激。

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

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.

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来源期刊

Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY

CiteScore

8.00

自引率

3.40%

发文量

200

期刊介绍： Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]