Pseudoginsenoside-F11 Accelerates Microglial Phagocytosis of Myelin Debris and Attenuates Cerebral Ischemic Injury Through Complement Receptor 3

Liu, Yinglu; Wu, Chunfu; Hou, Zongjuan; Fu, Xiaoxiao; Yuan, Linlin; Sun, Shibo; Zhang, Haotian; Yang, Depeng; Yao, Xuechun; Yang, Jingyu

doi:10.1016/j.neuroscience.2019.11.010

Cited by 26 publications

(17 citation statements)

References 68 publications

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“…After the nylon suture was inserted into the CCA, the silk thread was tightened to ensure that the thread was able to pass through the artery without bleeding or loosening of the arterial clamp. The nylon suture was inserted into the CCA and ICA approximately 18–20 mm, and insertion was stopped when resistance was encountered [ 21 ]. The thread in the CCA was tightened, the incision was sutured, and the wound was disinfected.…”

Section: Methodsmentioning

confidence: 99%

Electroacupuncture Attenuates Inflammation after Ischemic Stroke by Inhibiting NF‐κB‐Mediated Activation of Microglia

Liu

Wei

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Microglial activation and microglia-mediated inflammation play an important role in the occurrence, development, and outcome of stroke. Brain injury induces the activation and release of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin- (IL-) 1β, and IL-6. Many studies have confirmed that acupuncture is effective in treating ischemic stroke. However, its protective mechanism against ischemic brain injury is complex and multifactorial. In this study, we observed the effects of electroacupuncture at Baihui (GV20) and Dazhui (GV14) on microglial activation and inflammation in the cortical ischemic penumbra (IP) of permanent middle cerebral artery occlusion (pMCAO) rats. It was found that electroacupuncture inhibited the degeneration and necrosis of microglia in the cortical IP and ameliorated mitochondrial damage. Immunofluorescence and western blot analysis showed that microglia were in a resting state or weakly activated in the normal brain. After cerebral ischemia, the expression of microglial markers (Iba-1 and CD11b) increased, and NF-κB p65, IL-1β, and TNF-α expression gradually increased. The dynamic changes were generally temporally consistent. Electroacupuncture downregulated the expressions of Iba-1 and CD11b. Additionally, it inhibited the expression of NF-κB p65, IL-1β, and TNF-α and reduced the conversion of microglia to the M1 phenotype after ischemia. Electroacupuncture regulated the activation of microglia and microglia-mediated inflammation after cerebral ischemia, confirming the relevant theories regarding the effect of acupuncture treatment on cerebral ischemia and guiding clinical practice.

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Section: Methodsmentioning

confidence: 99%

Electroacupuncture Attenuates Inflammation after Ischemic Stroke by Inhibiting NF‐κB‐Mediated Activation of Microglia

Liu

Wei

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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“…For example, deletion of Na + /H + exchanger, Nhe1, in microglia/macrophages successfully promotes the expression of anti‐inflammatory cytokines, including Ym1, TGF‐β, and IL‐10, which subsequently stimulates white matter remyelination at 14 days after stroke 126 . In addition, the phagocytic capabilities of microglia/macrophages enable engulfment of myelin debris and provide neuroprotection in stroke 127 . In an experimental ICH model, white matter fibers within the hematoma may be used by microglia/macrophages as a scaffold to infiltrate into the hematoma and assist in its clearance 128 …”

Section: Diverse Functions Of Activated Microglia/macrophages In Strokementioning

confidence: 99%

Microglial/Macrophage polarization and function in brain injury and repair after stroke

et al. 2021

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Stroke is a leading cause of disability and mortality, with limited treatment options. After stroke injury, microglia and CNS‐resident macrophages are rapidly activated and regulate neuropathological processes to steer the course of functional recovery. To accelerate this recovery, microglia can engulf dying cells and clear irreparably‐damaged tissues, thereby creating a microenvironment that is more suitable for the formation of new neural circuitry. In addition, monocyte‐derived macrophages cross the compromised blood‐brain barrier to infiltrate the injured brain. The specific functions of myeloid lineage cells in brain injury and repair are diverse and dependent on phenotypic polarization statuses. However, it remains to be determined to what degree the CNS‐invading macrophages occupy different functional niches from CNS‐resident microglia. In this review, we describe the physiological characteristics and functions of microglia in the developing and adult brain. We also review (a) the activation and phenotypic polarization of microglia and macrophages after stroke, (b) molecular mechanisms that control polarization status, and (c) the contribution of microglia to brain pathology versus repair. Finally, we summarize current breakthroughs in therapeutic strategies that calibrate microglia/macrophage responses after stroke.

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“…However, Tat-CX3CL1 (357-395aa) did not affect mice swimming speed (Fig 6C). Moreover, neuroin ammation induced by ischemic cerebral damage may be facilitate the loss of myelin sheath and white matter lesions [35].…”

Section: Resultsmentioning

confidence: 99%

Blocking PSD-93-CX3CL1 Interaction Promotes Phenotypic Polarization Transformation of Microglia During Acute Ischemic Stroke Injury

Zhang¹,

Cao²,

Yang³

et al. 2021

Preprint

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Background：Postsynaptic density 93 (PSD-93) plays an important role in ischemic brain injury through mediating neurotoxicity and neuroinflammation. Blocked the combination of PSD-93 and Fractalkine (CX3Cchemokineligand1, CX3CL1) play beneficial roles in acute ischemic stroke. However, the underlying mechanism still need further exploration. Methods：In this study, male C57BL/6 mice aged 8-12 weeks and weighted 22-26g were applied with Middle Cerebral Artery Occlusion (MCAO) model and randomly divided into different groups. Firstly, real-time quantitative PCR was to detect some cytokines associated with M1 and M2 type of microglia at different time points in transient MCAO model. Secondly, triphenyl tetrazolium chloride (TTC) staining, brain water content and behavioral assessments were used to evaluate the neurologic damage. Immunofluorescence staining was performed to measure the white matter injury, and microglia polarization. Moreover, enzyme-linked immunosorbent assay (ELISA) was used to investigate the expression of soluble CX3CL1. Results：M1 phenotype cytokines were detected at different time points and found that their expression increased from beginning at 6 hours after reperfusion and most peaked at 24 h after reperfusion. However, the expression of M2 phenotype cytokines decreased or still keep invariant at 6 hours and 24 h after reperfusion. Interestingly, Tat-CX3CL1 (357-395aa) can facilitate microglia polarization from M1 type to M2 type through inhibiting expression of the soluble CX3CL1. Furthermore, CX3CL1 specific cleavase inhibitor ADAM17 could restrain the microglia polarization transformation via reducing the soluble CX3CL1 formation. Moreover, Tat-CX3CL1 (357-395aa) also attenuate long-term cognitive deficits and improved white matter integrity. Conclusions: In conclusion, we demonstrated that specific blockage the binding of PSD-93 and CX3CL1 by Tat-CX3CL1 (357-395aa) could perform functional recovery after ischemic stroke by promoting type microglia polarization transformation from M1 to M2. And the peptide Tat-CX3CL1 (357-395aa) is a promising strategy for treatment of ischemic stroke.

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Pseudoginsenoside-F11 Accelerates Microglial Phagocytosis of Myelin Debris and Attenuates Cerebral Ischemic Injury Through Complement Receptor 3

Cited by 26 publications

References 68 publications

Electroacupuncture Attenuates Inflammation after Ischemic Stroke by Inhibiting NF‐κB‐Mediated Activation of Microglia

Electroacupuncture Attenuates Inflammation after Ischemic Stroke by Inhibiting NF‐κB‐Mediated Activation of Microglia

Microglial/Macrophage polarization and function in brain injury and repair after stroke

Blocking PSD-93-CX3CL1 Interaction Promotes Phenotypic Polarization Transformation of Microglia During Acute Ischemic Stroke Injury

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