Quantitative analysis of influence of sevoflurane on the reactivity of microglial cells in the course of the experimental model of intracerebral haemorrhage

Karwacki, Zbigniew; Kowiański, Przemysław; Dziewíatkowski, J; Domaradzka-Pytel, B; Ludkiewicz, Beata; Wójcik, Sławomir; Narkiewicz, O; Moryś, Janusz

doi:10.1017/s0265021506000603

Cited by 14 publications

(17 citation statements)

References 26 publications

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“…Our data show that after IR injury, microglia were rapidly activated in IR group rats, as cells were intensely stained with Iba-1 antibody and possessed enlarged and vacuolated cell bodies extending stout processes (Figure 4A). Sevoflurane preconditioning markedly prevented increases in Iba-1 protein expression (Figure 5A), completely consistent with the results of Karwacki Z and colleagues [30]. …”

Section: Discussionsupporting

confidence: 91%

“…Karwacki Z and colleagues reported that sevoflurane in concentrations of 1 and 2 MAC (minimum alveolar concentration) inhibited ischemia-induced polymorphonuclear neutrophil (PMN) adhesion. With similar immunophenotypical features as those of PMN, sevoflurane was demonstrated to modulate microglial adhesion [30]. Herein, we used Iba-1 as cellular marker of microglia and analyzed microglial activation qualitatively and quantitatively.…”

Section: Discussionmentioning

confidence: 99%

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Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

Cao

Wang

et al. 2014

Mol Brain

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BackgroundMicroglia are the primary immune cells of the spinal cord that are activated in response to ischemia/reperfusion (IR) injury and release various neurotrophic and/or neurotoxic factors to determine neuronal survival. Among them, matrix metalloproteinase-9 (MMP-9), which cleaves various components of the extracellular matrix in the basal lamina and functions as part of the blood spinal cord barrier (BSCB), is considered important for regulating inflammatory responses and microenvironmental homeostasis of the BSCB in the pathology of ischemia. Sevoflurane has been reported to protect against neuronal apoptosis during cerebral IR. However, the effects of sevoflurane preconditioning on spinal cord IR injury remain unclear. In this study, we investigated the role of sevoflurane on potential genetic roles of microglial MMP-9 in tight junction protein breakdown, opening of the BSCB, and subsequent recruitment of microglia to apoptotic spinal cord neurons.ResultsThe results showed significant upregulation of MMP-9 in rats with IR-induced inflammation of the BSCB compared to that of the sham group, manifested as dysfunctional BSCB with increased Evans blue extravasation and reduced expression of occludin protein. Increased MMP-9 expression was also observed to facilitate invasion and migration of activated microglia, imaging as high Iba-1 expression, clustered to neurons in the injured spinal cord, as shown by double immunofluorescence, and increased proinflammatory chemokine production (CXCL10, CCL2). Further, sevoflurane preconditioning markedly improved motor function by ameliorating neuronal apoptosis, as shown by reduced TUNEL-positive cell counts and expression of cleaved caspase-3. These protective effects were probably responsible for downregulation of MMP-9 and maintenance of normal expression of occludin protein indicating BSCB integrity from inflammatory damage, which was confirmed by decreased protein levels of Iba-1 and MMP-9, as well as reduced production of proinflammatory chemokines (CXCL10, CCL2) and proinflammatory cytokines (IL-1β). Intrathecal injection of specific siRNAs targeting MMP-9 had similar protective effects to those of sevoflurane preconditioning.ConclusionsPreconditioning with 2.4% sevoflurane attenuated spinal cord IR injury by inhibiting recruitment of microglia and secretion of MMP-9; thus inhibiting downstream effects on inflammatory damage to BSCB integrity and neuronal apoptosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-014-0069-7) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

Cao

Wang

et al. 2014

Mol Brain

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“…The control group comprised of animals that underwent the same surgical procedure as rats that were subjected to intracerebral haematoma (described below) with the exception of blood injection. In the study we used the experimental model of intracerebral haemorrhage described previously by Karwacki et al [15][16][17] where detailed description of anaesthetic and surgical procedures were presented. Here we provide brief description of the experimental procedures used.…”

Section: Animal Proceduresmentioning

confidence: 99%

Minocycline but not valproic acid influence the density of NogoA-immunoreactive neurons in the hilus of the dentate gyrus of the rats subjected to intracerebral haematoma

et al. 2014

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“…Temperature commonly decreases following anesthesia in small animals, principally due to their high surface area-to-body mass ratio making thermo- Harvey and Paddleford, 1993;Karwacki et al, 2005Karwacki et al, , 2006aKiyatkin and Brown, 2005. regulation difficult. The use of unwarmed anesthetic gases exacerbates this problem (Haskins and Patz, 1980).…”

Section: Minimizing Excess Inflammationmentioning

confidence: 99%

Experimental Intracerebral Hemorrhage: Avoiding Pitfalls in Translational Research

Kirkman

Allan

Parry‐Jones

2011

J Cereb Blood Flow Metab

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Intracerebral hemorrhage (ICH) has the highest mortality of all stroke subtypes, yet treatments are mainly limited to supportive management, and surgery remains controversial. Despite significant advances in our understanding of ICH pathophysiology, we still lack preclinical models that accurately replicate the underlying mechanisms of injury. Current experimental ICH models (including autologous blood and collagenase injection) simulate different aspects of ICH-mediated injury but lack some features of the clinical condition. Newly developed models, notably hypertension-and oral anticoagulant therapy-associated ICH models, offer added benefits but further study is needed to fully validate them. Here, we describe and discuss current approaches to experimental ICH, with suggestions for changes in how this condition is studied in the laboratory. Although advances in imaging over the past few decades have allowed greater insight into clinical ICH, there remains an important role for experimental models in furthering our understanding of the basic pathophysiologic processes underlying ICH, provided limitations of animal models are borne in mind. Owing to differences in existing models and the failed translation of benefits in experimental ICH to clinical practice, putative neuroprotectants should be trialed in multiple models using both histological and functional outcomes until a more accurate model of ICH is developed.

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Quantitative analysis of influence of sevoflurane on the reactivity of microglial cells in the course of the experimental model of intracerebral haemorrhage

Abstract: Administration of sevoflurane during anaesthesia in animals with intracerebral haemorrhage evoked a decrease of activation of the microglial cells.

Cited by 14 publications

References 26 publications

Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

Minocycline but not valproic acid influence the density of NogoA-immunoreactive neurons in the hilus of the dentate gyrus of the rats subjected to intracerebral haematoma

Experimental Intracerebral Hemorrhage: Avoiding Pitfalls in Translational Research

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