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ORIGINAL RESEARCH article

Front. Cell. Infect. Microbiol.
Sec. Intestinal Microbiome
Volume 14 - 2024 | doi: 10.3389/fcimb.2024.1413018

Significance of the gut tract in the therapeutic mechanisms of polydopamine for acute cerebral infarction: neuro-immune interaction through the gut-brain axis

Provisionally accepted
Fenghua Xu Fenghua Xu 1Xiao Sun Xiao Sun 1Ling-Yang Kong Ling-Yang Kong 1Wen-Xiang Hui Wen-Xiang Hui 1Jun Zhu Jun Zhu 2Cong-Peng Zhang Cong-Peng Zhang 1Yi-Ming Cheng Yi-Ming Cheng 1Wen-Xin Han Wen-Xin Han 1Zhimin Tian Zhimin Tian 3Yan-Ning Qiao Yan-Ning Qiao 1Lei Liu Lei Liu 4*Dayun Feng Dayun Feng 5*Jing Han Jing Han 1*
  • 1 Shaanxi Normal University, Xi'an, China
  • 2 Xijing Hospital, Air Force Medical University, Xi’an, Shaanxi Province, China
  • 3 Northwestern Polytechnical University, Xi'an, Shaanxi Province, China
  • 4 Army Medical University, Chongqing, China
  • 5 Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi Province, China

The final, formatted version of the article will be published soon.

    Background: Recent research has made significant progress in elucidating gastrointestinal complications following acute cerebral infarction (ACI), which includes disorders in intestinal motility and dysbiosis of the gut microbiota. Nevertheless, the role of the gut (which is acknowledged as being the largest immune organ) in the immunoreactive effects of polydopamine nanoparticles (PDA) on acute ischaemic stroke remains inadequately understood. In addition to its function in nutrient absorption, the gut acts as a protective barrier against microbes. Systemic immune responses, which are triggered by the disruption of gut barrier integrity, are considered as one of the mechanisms underlying acute ischaemic stroke, with the gut-brain axis (GBA) playing a pivotal role in this process.In this study, we used a PDA intervention in an ACI model to investigate ACI-like behaviour, intestinal barrier function, central and peripheral inflammation, and hippocampal neuron excitability, thus aiming to elucidate the mechanisms through which PDA improves ACI via the GBA.Results: Our findings indicated that as ACI mice experienced dysbiosis of the gut microbiota and intestinal barrier damage, the levels of proinflammatory factors in the serum and brain significantly increased. Additionally, the activation of astrocytes in the hippocampal region and neuronal apoptosis were observed in ACI mice. Importantly, our study is the first to provide evidence demonstrating that PDA effectively suppresses the neuroimmune interactions of the gutbrain axis and significantly improves intestinal epithelial barrier integrity.We hope that our discoveries will serve as a foundation for further explorations of the therapeutic mechanisms of PDA in ACI, particularly in elucidating the protective roles of gut microbiota and intestinal barrier function, as well as in the development of more targeted clinical interventions for ACI.

    Keywords: Acute cerebral infarction, brain-gut axis, polydopamine, Reactive Oxygen Species, inflammatory responses

    Received: 06 Apr 2024; Accepted: 25 Nov 2024.

    Copyright: © 2024 Xu, Sun, Kong, Hui, Zhu, Zhang, Cheng, Han, Tian, Qiao, Liu, Feng and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Lei Liu, Army Medical University, Chongqing, 400038, China
    Dayun Feng, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi Province, China
    Jing Han, Shaanxi Normal University, Xi'an, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.