Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
CNS Neurol Disord Drug Targets. 2021;20(5):401-416. doi: 10.2174/1871527320666210322115808.
The gastrointestinal tract is a major organ of the body that absorbs nutrients, water, and electrolytes. At the same time, it is a tight barrier that resists the invasion of harmful substances and maintains the homeostasis of the internal environment. Destruction of the intestinal barrier is linked to the digestive system, cardiovascular system, endocrine system, and other systemic diseases. Mounting evidence suggests that ischemic stroke not only changes the intestinal microbes but also increases the permeability of the intestinal barrier, leading to bacterial translocation, infection, and even sepsis. The intestinal barrier, as part of the gut-brain axis, has also been proven to participate in the pathophysiological process of ischemic stroke. However, little attention has been paid to it. Since ischemic stroke is a major public health issue worldwide, there is an urgent need to know more about the disease for better prevention, treatment, and prognosis. Therefore, understanding the pathophysiological relationship between ischemic stroke and the intestinal barrier will help researchers further uncover the pathophysiological mechanisms of ischemic stroke and provide a novel therapeutic target for the treatment of ischemic stroke. Here, we review the physiology and pathology between ischemic stroke and intestinal barrier based on related articles published in the past ten years about the relationship between ischemic stroke, stroke risk factors and intestinal flora, and intestinal barrier. We further discuss the following parts: the intestinal barrier, possible mechanisms of intestinal barrier destruction in ischemic stroke, intestinal barrier destruction caused by stroke-related risk factors, intestinal barrier dysfunction in ischemic stroke, targeting the intestinal barrier for improving stroke, conclusions and perspectives.
胃肠道是人体主要的器官之一，它吸收营养物质、水分和电解质。同时，它也是一个紧密的屏障，能够抵御有害物质的入侵，维持内环境的稳定。肠道屏障的破坏与消化系统、心血管系统、内分泌系统等全身性疾病有关。越来越多的证据表明，缺血性脑卒中不仅改变了肠道微生物群，还增加了肠道屏障的通透性，导致细菌易位、感染，甚至脓毒症。肠道屏障作为肠-脑轴的一部分，已被证明参与了缺血性脑卒中的病理生理过程。然而，目前对此关注较少。由于缺血性脑卒中是全球范围内的一个主要公共卫生问题，因此需要更多地了解这种疾病，以实现更好的预防、治疗和预后。因此，了解缺血性脑卒中与肠道屏障之间的病理生理关系，将有助于研究人员进一步揭示缺血性脑卒中的病理生理机制，并为缺血性脑卒中的治疗提供新的治疗靶点。在这里，我们根据过去十年中关于缺血性脑卒中、脑卒中风险因素与肠道菌群以及肠道屏障之间关系的相关文章，综述了缺血性脑卒中与肠道屏障之间的生理学和病理学关系。我们进一步讨论了以下几个部分：肠道屏障、缺血性脑卒中时肠道屏障破坏的可能机制、与脑卒中相关的风险因素引起的肠道屏障破坏、缺血性脑卒中时的肠道屏障功能障碍、针对肠道屏障改善脑卒中的治疗、结论和展望。
