Exploring the anti-ferroptosis mechanism of Kai-Xin-San against Alzheimer's disease through integrating network pharmacology, bioinformatics, and experimental validation strategy in vivo and in vitro

Yan, Chenchen; Yang, Song; Shao, Simai; Zu, Runru; Lu, Hao; Chen, Yuanzhao; Zhou, Yangang; Ying, Xiran; Xiang, Shixie; Zhang, Peixu; Li, Zhonghua; Yuan, Ye; Zhang, Zhenqiang; Wang, Pan; Xie, Zhishen; Wang, Wang; Ma, Huifen; Sun, Yiran

doi:10.1016/j.jep.2024.117915

Cited by 3 publications

(1 citation statement)

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“…Abbreviations: AA, arachidonic acid; AMPK, adenosine 5'-monophosphate (AMP)-activated protein kinase; ARE, antioxidant responseelement; FPN, ferroportin; Fth, ferritin heavy; GPX4, glutathione peroxidase 4; GSH, glutathione; GSSG, oxidized glutathione; HMGB1, high mobility group protein B1; HO-1, heme oxygenase 1; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; MyD88, Myeloid Differentiation Factor 88; NF-κB, nuclear factor-kappaB; Nrf2, nuclear factor erythroid-2-related factor 2; PGs, prostaglandins; PGC-1α, PPAR-γ Coactivator 1 alpha; ROS, reactive oxygen species; SIRT1, silent information regulator 1; STING, stimulator of interferon genes; TBK-1, TANK-binding kinase 1; TLR4, Toll-like receptor Furthermore, SIRT1 has been found to inhibit ferroptosis in nerve cells through a non-GPX4-dependent ferroptosis protection pathway. In experiments with HT22 cells in vivo and in vitro in Alzheimer's mice, Jiatong Zhang and Wei Li's team demonstrated that the upregulation of SIRT1 in AD inhibits ferroptosis via the FSP1 axis [86]. Similar results were observed in a study on subarachnoid hemorrhage [87].…”

Section: The Link Between Neuroinflammation and Ferroptosismentioning

confidence: 55%

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Xu,

Jia,

et al. 2024

Antioxidants

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Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers’ findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders.

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Section: The Link Between Neuroinflammation and Ferroptosismentioning

confidence: 55%

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Xu,

Jia,

et al. 2024

Antioxidants

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Progress of Exosomal MicroRNAs and Traditional Chinese Medicine Monomers in Neurodegenerative Diseases

Liang,

Zhu,

Liu

et al. 2024

Phytotherapy Research

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Exosomes, extracellular vesicles secreted by various cells, actively participate in intercellular communication by facilitating the exchange of crucial molecular information such as DNA, RNA, and lipids. Within this intricate network, microRNAs, endogenous non‐coding small RNAs, emerge as pivotal regulators of post‐transcriptional gene expression, significantly influencing the development of neurodegenerative diseases. The historical prominence of traditional Chinese medicine (TCM) in clinical practice in China underscores its enduring significance. Notably, TCM monomers, serving as active constituents within herbal medicine, assume a critical role in the treatment of neurodegenerative diseases, particularly in mitigating oxidative stress, inhibiting apoptosis, and reducing inflammation. This comprehensive review aims to delineate the specific involvement of exosomal microRNAs in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke, and amyotrophic lateral sclerosis. Furthermore, the exploration extends to the application of TCM monomers, elucidating their efficacy as therapeutic agents in these conditions. Additionally, the review examines the utilization of exosomes as drug delivery carriers in the context of neurodegenerative diseases, providing a nuanced understanding of the potential synergies between TCM and modern therapeutic approaches. This synthesis of knowledge aims to contribute to the advancement of our comprehension of the intricate molecular mechanisms underlying neurodegeneration and the potential therapeutic avenues offered by TCcom interventions.

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Kaixinsan regulates neuronal mitochondrial homeostasis to improve the cognitive function of Alzheimer's disease by activating CaMKKβ-AMPK-PGC-1α signaling axis

Ren,

Xiang,

Song

et al. 2024

Phytomedicine

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Exploring the anti-ferroptosis mechanism of Kai-Xin-San against Alzheimer's disease through integrating network pharmacology, bioinformatics, and experimental validation strategy in vivo and in vitro

Cited by 3 publications

References 51 publications

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Progress of Exosomal MicroRNAs and Traditional Chinese Medicine Monomers in Neurodegenerative Diseases

Kaixinsan regulates neuronal mitochondrial homeostasis to improve the cognitive function of Alzheimer's disease by activating CaMKKβ-AMPK-PGC-1α signaling axis

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