Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway

Cai, Min; Sun, Sisi; Wang, Jin; Dong, Beibei; Yang, Qianzi; Tian, Li; Dong, Hailong; Wang, Shiquan; Hou, Wugang

doi:10.1111/cns.13715

Cited by 37 publications

(34 citation statements)

References 58 publications

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“…Hypoxic preconditioning-induced Nrf2 activation occurs in a GSK-3β phosphorylation-dependent manner and enhances anti-inflammatory microglia phenotype polarization after cerebral I/R, thus favoring ischemic tolerance and protective processes (Cai et al, 2021 ). Furthermore, ischemic/hypoxic conditioning therapeutics can influence microglia dynamics, including migration, phagocytosis, and proliferation at early stages after brain ischemia and reperfusion, promoting brain repair (Dang et al, 2018 ).…”

Section: Microglia a Promising Target For Neuroprotection In Ischemic...mentioning

confidence: 99%

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Wang

Leak

Cao

2022

Front. Cell. Neurosci.

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Stroke remains a major cause of long-term disability and mortality worldwide. The immune system plays an important role in determining the condition of the brain following stroke. As the resident innate immune cells of the central nervous system, microglia are the primary responders in a defense network covering the entire brain parenchyma, and exert various functions depending on dynamic communications with neurons, astrocytes, and other neighboring cells under both physiological or pathological conditions. Microglia activation and polarization is crucial for brain damage and repair following ischemic stroke, and is considered a double-edged sword for neurological recovery. Microglia can exist in pro-inflammatory states and promote secondary brain damage, but they can also secrete anti-inflammatory cytokines and neurotrophic factors and facilitate recovery following stroke. In this review, we focus on the role and mechanisms of microglia-mediated neuroinflammation and neuroplasticity after ischemia and relevant potential microglia-based interventions for stroke therapy.

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Section: Microglia a Promising Target For Neuroprotection In Ischemic...mentioning

confidence: 99%

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Wang

Leak

Cao

2022

Front. Cell. Neurosci.

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“…48,49 Therapeutic effects include a reduction in lesion volume, improvement of functional outcome, 50 attenuation of reactive astrogliosis, 51 and promotion of anti-inflammatory microglial and macrophage phenotypes. 52 Research revealed numerous molecular pathways that mediate the beneficial effects of volatile anesthetics.…”

Section: Inhalative Substancesmentioning

confidence: 99%

Perioperative stroke: A perspective on challenges and opportunities for experimental treatment and diagnostic strategies

Jin

Michalski

et al. 2022

CNS Neurosci Ther

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Perioperative stroke is an ischemic or hemorrhagic cerebral event during or up to 30 days after surgery. It is a feared condition due to a relatively high incidence, difficulties in timely detection, and unfavorable outcome compared to spontaneously occurring stroke. Recent preclinical data suggest that specific pathophysiological mechanisms such as aggravated neuroinflammation contribute to the detrimental impact of perioperative stroke. Conventional treatment options are limited in the perioperative setting due to difficult diagnosis and medications affecting coagulation in may cases. On the contrary, the chance to anticipate cerebrovascular events at the time of surgery may pave the way for prevention strategies. This review provides an overview on perioperative stroke incidence, related problems, and underlying pathophysiological mechanisms. Based on this analysis, we assess experimental stroke treatments including neuroprotective approaches, cell therapies, and conditioning medicine strategies regarding their potential use in perioperative stroke. Interestingly, the specific aspects of perioperative stroke might enable a more effective application of experimental treatment strategies such as classical neuroprotection whereas others including cell therapies may be of limited use. We also discuss experimental diagnostic options for perioperative stroke augmenting classical clinical and imaging stroke diagnosis. While some experimental stroke treatments may have specific advantages in perioperative stroke, the paucity of established guidelines or multicenter clinical research initiatives currently limits their thorough investigation.

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“…Receptors, signaling pathways and transcription factors also influence macrophage polarization. Sevoflurane pretreatment promotes the formation of an anti-inflammatory phenotype in microglia/macrophages by up-regulating the phosphorylation of GSK-3β and Nrf2 nuclear transposition, and it has a neuroprotective effect on middle cerebral artery occlusion (MCAO) ( Cai et al, 2021a ). However, sevoflurane inhibits FoxO1, regulates p21 and increases the expression of TNF-α, monocyte chemotactic protein-1 (MCP-1) and IL-6, which may increase the polarization of M1 macrophages, induce a central nervous system (CNS) inflammatory response, and lead to cognitive impairment ( Fu et al, 2020 ).…”

Section: Macrophages and Anestheticmentioning

confidence: 99%

“…Dexmedetomidine and propofol inhibit the expression of lipopolysaccharide (LPS)-stimulated high mobility group box 1 (HMGB1) in macrophages ( Chang et al, 2013 ; Jia et al, 2017 ). The volatile anesthetic sevoflurane modulates macrophage recruitment, polarization, differentiation, apoptosis and pyroptosis by regulating the caspase-1, reactive oxygen species (ROS), forkhead box O1 (FoxO1), p21, and glycogen synthase kinase-3 (GSK-3β)/nuclear factor-E2-related factor 2 (Nrf2) pathways, which are involved in local immunity and tumor growth ( Jin et al, 2013 ; Fu et al, 2020 ; Sztwiertnia et al, 2020 ; Cai et al, 2021a ). Opioids, such as morphine, also inhibit the phagocytosis of macrophages and are associated with the reduction of macrophage colony-stimulating factor-induced proliferation and differentiation ( Sacerdote et al, 2003 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of propofol on macrophage activation and function in diseases

Tao

Wang

et al. 2022

Front. Pharmacol.

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Macrophages work with monocytes and dendritic cells to form a monocyte immune system, which constitutes a powerful cornerstone of the immune system with their powerful antigen presentation and phagocytosis. Macrophages play an essential role in infection, inflammation, tumors and other pathological conditions, but these cells also have non-immune functions, such as regulating lipid metabolism and maintaining homeostasis. Propofol is a commonly used intravenous anesthetic in the clinic. Propofol has sedative, hypnotic, anti-inflammatory and anti-oxidation effects, and it participates in the body’s immunity. The regulation of propofol on immune cells, especially macrophages, has a profound effect on the occurrence and development of human diseases. We summarized the effects of propofol on macrophage migration, recruitment, differentiation, polarization, and pyroptosis, and the regulation of these propofol-regulated macrophage functions in inflammation, infection, tumor, and organ reperfusion injury. The influence of propofol on pathology and prognosis via macrophage regulation is also discussed. A better understanding of the effects of propofol on macrophage activation and function in human diseases will provide a new strategy for the application of clinical narcotic drugs and the treatment of diseases.

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Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 37 publications

References 58 publications

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Perioperative stroke: A perspective on challenges and opportunities for experimental treatment and diagnostic strategies

Effects of propofol on macrophage activation and function in diseases

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