Minimally invasive surgery for ICH evacuation followed by rosiglitazone infusion therapy increased perihematomal PPARγ expression and improved neurological outcomes in rabbits

Wu, Guofeng; Wu, Junjie; Wang, Likun; Jiao, Yu; Zhou, Houguang; Tang, Zhouping

doi:10.1080/01616412.2015.1105627

Cited by 8 publications

(4 citation statements)

References 33 publications

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“…NF-kB activation is regulated by the PPAR transcription factors (Deng et al, 2016). PPARγ, the most studied PPAR isoform, has shown the most potent neuroprotective effects in different models of neurodegenerative disorders such as I/R-induced brain injury and AD (Zhao et al, 2006; Zolezzi et al, 2014; Wu et al, 2016; Chen et al, 2018). Consistent with this, co-treatment of the MCAO rats with 1, 25-D 3 and a PPARγ inhibitor blocked the protective effects of the former, on brain injury (Grommes et al, 2013; Wang et al, 2016; Chen et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: 1, 25-D3 Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation

Guo

Wang

Guo

et al. 2018

Front. Cell. Neurosci.

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The blood-brain barrier (BBB) is a physical and biochemical barrier that maintains cerebral homeostasis. BBB dysfunction in an ischemic stroke, results in brain injury and subsequent neurological impairment. The aim of this study was to determine the possible protective effects of 1, 25-dihydroxyvitamin D3 [1, 25(OH)2D3, 1, 25-D3, vit D] on BBB dysfunction, at the early stages of an acute ischemic brain injury. We analyzed the effects of 1, 25-D3 on BBB integrity in terms of histopathological changes, the neurological deficit, infarct size and the expression of brain derived neurotrophic factor (BDNF), in a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model. BBB permeability and the expression of permeability-related proteins in the brain were also evaluated by Evans blue (EB) staining and Western blotting respectively. To determine the possible mechanism underlying the role of 1, 25-D3 in BBB maintenance, after MCAO/R, the rats were treated with the specific peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662. Supplementation with 1, 25-D3 markedly improved the neurological scores of the rats, decreased the infarct volume, prevented neuronal deformation and upregulated the expression of the tight junction (TJ) and BDNF proteins in their brains. Furthermore, it activated PPARγ but downregulated neuro-inflammatory cytokines such as nuclear factor kappa-B (NF-κB) and tumor necrosis factor-α (TNF-α), after MCAO/R. Taken together, 1, 25-D3 protects against cerebral ischemia by maintaining BBB permeability, upregulating the level of BDNF and inhibiting PPARγ-mediated neuro-inflammation.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: 1, 25-D3 Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation

Guo

Wang

Guo

et al. 2018

Front. Cell. Neurosci.

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“…We also showed that the use of rosiglitazone can relieve secondary brain injury [8][9]. Although the mechanism is still unclear, it has been shown that rosiglitazone acts as a specific agonist of PPARγ and regulates downstream genes through multiple signaling pathways, such as the pathways of PPARγ, Ras-Raf-MAPK, Transforming Growth Factor (TGF), and β-Catenin.…”

Section: Introductionmentioning

confidence: 94%

Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPARγ and CD36

Wang

Hang

et al. 2017

Neuroscience Letters

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“…Clinical evidence shows that hematoma size and expansion are the major determinants of ICH outcomes (Brott et al, 1997; LoPresti et al, 2014). Until now, however, little preclinical work has evaluated potential strategies to limit hematoma expansion or accelerate hematoma resolution after ICH (Flores et al, 2016; King et al, 2011; Wu et al, 2016; Zhao et al, 2015b; Zhao et al, 2007b). …”

Section: Introductionmentioning

confidence: 99%

Alternative activation-skewed microglia/macrophages promote hematoma resolution in experimental intracerebral hemorrhage

Chang

Wan

et al. 2017

Neurobiology of Disease

113

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Microglia/macrophages (MMΦ) are highly plastic phagocytes that can promote both injury and repair in diseased brain through the distinct function of classically activated and alternatively activated subsets. The role of MMΦ polarization in intracerebral hemorrhage (ICH) is unknown. Herein, we comprehensively characterized MMΦ dynamics after ICH in mice and evaluated the relevance of MMΦ polarity to hematoma resolution. MMΦ accumulated within the hematoma territory until at least 14 days after ICH induction. Microglia rapidly reacted to the hemorrhagic insult as early as 1–1.5 h after ICH and specifically presented a “protective” alternatively activated phenotype. Substantial numbers of activated microglia and newly recruited monocytes also assumed an early alternatively activated phenotype, but the phenotype gradually shifted to a mixed spectrum over time. Ultimately, markers of MMΦ classic activation dominated at the chronic stage of ICH. We enhanced MMΦ alternative activation by administering intraperitoneal injections of rosiglitazone, and subsequently observed elevations in CD206 expression on brain-isolated CD11b+ cells and increases in IL-10 levels in serum and perihematomal tissue. Enhancement of MMΦ alternative activation correlated with hematoma volume reduction and improvement in neurologic deficits. Intraventricular injection of alternative activation signature cytokine IL-10 accelerated hematoma resolution, whereas microglial phagocytic ability was abolished by IL-10 receptor neutralization. Our results suggest that MMΦ respond dynamically to brain hemorrhage by exhibiting diverse phenotypic changes at different stages of ICH. Alternative activation-skewed MMΦ aid in hematoma resolution, and IL-10 signaling might contribute to regulation of MMΦ phagocytosis and hematoma clearance in ICH.

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Minimally invasive surgery for ICH evacuation followed by rosiglitazone infusion therapy increased perihematomal PPARγ expression and improved neurological outcomes in rabbits

Abstract: Performing MIS followed by PPARγ agonist infusion therapy is more efficacious for reducing secondary damage to the brain and improving neurological function.

Cited by 8 publications

References 33 publications

RETRACTED: 1, 25-D3 Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation

RETRACTED: 1, 25-D3 Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation

Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPARγ and CD36

Alternative activation-skewed microglia/macrophages promote hematoma resolution in experimental intracerebral hemorrhage

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