The Neuroprotective Effect of Irisin in Ischemic Stroke

Liu, Yaqiang; Zhu, Changlian; Guo, Jiahui; Chen, Yonghong; Meng, Chaoyue

doi:10.3389/fnagi.2020.588958

Cited by 24 publications

(20 citation statements)

References 87 publications

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“…Recently, the anti-inflammatory, anti-apoptotic and anti-oxidative properties of irisin have received a great deal of attention in various diseases [ 22 ]. Previous studies explored the critical role that irisin played in ischemic stroke in mice models, indicating that irisin can upregulate the levels of brain-derived neurotrophic factor (BDNF) and protects nerve cells from injury during ischemic stroke [ 46 , 47 ]. Clinical investigations revealed that decreased serum concentration of irisin is associated with poor functional outcomes and post-stroke depression in ischemic stroke patients [ 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Irisin ameliorates neuroinflammation and neuronal apoptosis through integrin αVβ5/AMPK signaling pathway after intracerebral hemorrhage in mice

Wang

Tian

Tan

et al. 2022

J Neuroinflammation

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Background Neuroinflammation is a crucial factor in the development of secondary brain injury after intracerebral hemorrhage (ICH). Irisin is a newly identified myokine that confers strong neuroprotective effects in experimental ischemic stroke. However, whether this myokine can exert neuroprotection effects after ICH remains unknown. This study aimed to investigate the impact of irisin treatment on neuroinflammation and neuronal apoptosis and the underlying mechanism involving integrin αVβ5/AMPK pathway after ICH. Methods Two hundred and eighty-five adult (8-week-old) male C57BL/6 mice were randomly assigned to sham and ICH surgery groups. ICH was induced via intrastriatal injection of autologous blood. Irisin was administered intranasally at 30 min after ICH. To elucidate the underlying mechanism, cilengitide (a selective integrin αVβ5 inhibitor) and dorsomorphin (a selective phosphorylated AMPK inhibitor) were administered before irisin treatment. The short- and long-term neurobehavior tests, brain edema, quantitative-PCR, western blotting, Fluoro-Jade C, TUNEL, and immunofluorescence staining were performed to assess the neurofunctional outcome at the level of molecular, cell, histology, and function. Results Endogenous irisin and its receptor, integrin αVβ5, were increased, peaked at 24 h after ICH. irisin post-treatment improved both short- and long-term neurological functions, reduced brain edema after ICH. Interestingly, integrin αVβ5 was mainly located in the microglia after ICH, and irisin post-treatment inhibited microglia/macrophage pro-inflammatory polarization and promoted anti-inflammatory polarization. Moreover, irisin treatment inhibited neutrophil infiltration and suppressed neuronal apoptotic cell death in perihematomal areas after ICH. Mechanistically, irisin post-treatment significantly increased the expression of integrin αVβ5, p-AMPK and Bcl-2, and decreased the expression of IL-1β, TNF-α, MPO, and Bax following ICH. The neuroprotective effects of irisin were abolished by both integrin αVβ5 inhibitor cilengitide and AMPK inhibitor dorsomorphin. Conclusions This study demonstrated that irisin post-treatment ameliorated neurological deficits, reduced brain edema, and ameliorated neuroinflammation and neuronal apoptosis, at least in part, through the integrin αVβ5/AMPK signaling pathway after ICH. Thus, irisin post-treatment may provide a promising therapeutic approach for the early management of ICH.

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Section: Discussionmentioning

confidence: 99%

Irisin ameliorates neuroinflammation and neuronal apoptosis through integrin αVβ5/AMPK signaling pathway after intracerebral hemorrhage in mice

Wang

Tian

Tan

et al. 2022

J Neuroinflammation

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“…The most significant roles of irisin include browning of white adipocytes, neural proliferation, and bone metabolism [ 3 , 37 , 38 ]. Other effects of irisin involve glucose homeostasis and cardiac metabolism, which are still under investigation [ 4 ].…”

Section: The Role Of Irisin In Human Pathophysiologymentioning

confidence: 99%

FNDC5/Irisin: Physiology and Pathophysiology

et al. 2022

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A sedentary lifestyle or lack of physical activity increases the risk of different diseases, including obesity, diabetes, heart diseases, certain types of cancers, and some neurological diseases. Physical exercise helps improve quality of life and reduces the risk of many diseases. Irisin, a hormone induced by exercise, is a fragmented product of FNDC5 (a cell membrane protein) and acts as a linkage between muscles and other tissues. Over the past decade, it has become clear that irisin is a molecular mimic of exercise and shows various beneficial effects, such as browning of adipocytes, modulation of metabolic processes, regulation of bone metabolism, and functioning of the nervous system. Irisin has a role in carcinogenesis; numerous studies have shown its impact on migration, invasion, and proliferation of cancer cells. The receptor of irisin is not completely known; however, in some tissues it probably acts via a specific class of integrin receptors. Here, we review research from the past decade that has identified irisin as a potential therapeutic agent in the prevention or treatment of various metabolic-related and other diseases. This article delineates structural and biochemical aspects of irisin and provides an insight into the role of irisin in different pathological conditions.

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“…Под действием UCP1 повышается экспрессия мозгового нейротрофического фактора (brain-derived neurotrophic factor, BDNF) [17]. Показано, что введение irisin, высвобождение которого провоцируется снижением температуры, уменьшает объем инфаркта мозга у крыс после окклюзии среднемозговой артерии, стабилизирует гематоэнцефалический барьер и стимулирует накопление BDNF, уменьшает объем повреждений миокарда и легких после тотальной остановки кровообращения [18][19][20].…”

Section: молекулярные механизмы низкотемпературных технологийunclassified

Mechanisms of low-temperature rehabilitation technologies. Extreme aerocriotherapy

Шевелев

Petrova

Yuriev

et al. 2021

Physical and rehabilitation medicine, medical rehabilitation

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The mechanisms of increasing the resistance of cells to significant temperature and damaging effects are typical, and cellular tolerance, ensuring the effectiveness of systemic regulation, is an important part of increasing the adaptive and rehabilitative potential of the entire organism. The expression of early genes encoding a wide range of stress-protective proteins increases the resistance of cells not only to significant temperature stimuli, but also to ischemia, hypoxia, and other damaging factors, forming the effects of cross-adaptation. Even a small change in temperature is significant enough to trigger the processes of genomic reprogramming. It seems to us important to consider the mechanisms of low-temperature therapeutic and rehabilitation technologies from the standpoint of cellular response to temperature stimuli. Currently, a large number of low temperature technologies (HT) are used in medical rehabilitation, which can be divided into two groups: moderately low temperature effects (from 30C to +20C) and extremely low temperature effects (from 30C to 180C), which includes the technology of extreme aerocriotherapy (EACT). The purpose of the review is to analyze the systemic and local mechanisms of EACT implemented with the participation of the main known stress-protective proteins.

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The Neuroprotective Effect of Irisin in Ischemic Stroke

Cited by 24 publications

References 87 publications

Irisin ameliorates neuroinflammation and neuronal apoptosis through integrin αVβ5/AMPK signaling pathway after intracerebral hemorrhage in mice

Irisin ameliorates neuroinflammation and neuronal apoptosis through integrin αVβ5/AMPK signaling pathway after intracerebral hemorrhage in mice

FNDC5/Irisin: Physiology and Pathophysiology

Mechanisms of low-temperature rehabilitation technologies. Extreme aerocriotherapy

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