Emulsified isoflurane postconditioning improves survival and neurological outcomes in a rat model of cardiac arrest

Zhang, Yajie; M, Wu; Yu, Hai; Liu, Jin

doi:10.3892/etm.2017.4446

Cited by 6 publications

(2 citation statements)

References 39 publications

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“…Moreover, BTB09089 reduced the decrease of the density of neurons, while these effects disappeared in GPR65 −/− mice and reemerged when GPR65 was overexpressed in peri-infarct cortical neurons. Since neuronal apoptosis and necrosis are largely complete within 3 to 7 days poststroke in a progressive manner, [28][29][30] the reduction of decrease of the neuronal density may be attributed to the neuroprotective effect induced by BTB09089 applied at days 3 to 7 poststroke. This result is consistent with previously reported neuroprotective effects of BTB09089 in the acute phase of stroke.…”

Section: Discussionmentioning

confidence: 99%

Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke

Chen,

Zhang,

Miao

et al. 2024

Stroke

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BACKGROUND: GPR65 (G protein-coupled receptor 65) can sense extracellular acidic environment to regulate pathophysiological processes. Pretreatment with the GPR65 agonist BTB09089 has been proven to produce neuroprotection in acute ischemic stroke. However, whether delayed BTB09089 treatment and neuronal GPR65 activation promote neurorestoration remains unknown. METHODS: Ischemic stroke was induced in wild-type (WT) or GPR65 knockout (GPR65 −/− ) mice by photothrombotic ischemia. Male mice were injected intraperitoneally with BTB09089 every other day at days 3, 7, or 14 poststroke. AAV-Syn-GPR65 (adenoassociated virus-synapsin-GPR65) was utilized to overexpress GPR65 in the peri-infarct cortical neurons of GPR65 −/− and WT mice. Motor function was monitored by grid-walk and cylinder tests. The neurorestorative effects of BTB09089 were observed by immunohistochemistry, Golgi-Cox staining, and Western blotting. RESULTS: BTB09089 significantly promoted motor outcomes in WT but not in GPR65 −/− mice, even when BTB09089 was delayed for 3 to 7 days. BTB09089 inhibited the activation of microglia and glial scar progression in WT but not in GPR65 −/− mice. Meanwhile, BTB09089 reduced the decrease in neuronal density in WT mice, but this benefit was abolished in GPR65 −/− mice and reemerged by overexpressing GPR65 in peri-infarct cortical neurons. Furthermore, BTB09089 increased the GAP43 (growth-associated protein-43) and synaptophysin puncta density, dendritic spine density, dendritic branch length, and dendritic complexity by overexpressing GPR65 in the peri-infarct cortical neurons of GPR65 −/− mice, which was accompanied by increased levels of p-CREB (phosphorylated cAMP-responsive element-binding protein). In addition, the therapeutic window of BTB09089 was extended to day 14 by overexpressing GPR65 in the peri-infarct cortical neurons of WT mice. CONCLUSIONS: Our findings indicated that delayed BTB09089 treatment improved neurological functional recovery and brain tissue repair poststroke through activating neuronal GRP65. GPR65 overexpression may be a potential strategy to expand the therapeutic time window of GPR65 agonists for neurorehabilitation after ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke

Chen,

Zhang,

Miao

et al. 2024

Stroke

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“…The higher recognition index (RI = novel object interaction time/total object interaction time) demonstrates a better cognitive function. Emulsified isoflurane postconditioning improves ACA rat’s neurological outcomes, characterized by elevated RI ( Zhang et al, 2017 ).…”

Section: Neurologic Deficit Assessmentmentioning

confidence: 99%

Rat model of asphyxia-induced cardiac arrest and resuscitation

Zhu

et al. 2023

Front. Neurosci.

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Neurologic injury after cardiopulmonary resuscitation is the main cause of the low survival rate and poor quality of life among patients who have experienced cardiac arrest. In the United States, as the American Heart Association reported, emergency medical services respond to more than 347,000 adults and more than 7,000 children with out-of-hospital cardiac arrest each year. In-hospital cardiac arrest is estimated to occur in 9.7 per 1,000 adult cardiac arrests and 2.7 pediatric events per 1,000 hospitalizations. Yet the pathophysiological mechanisms of this injury remain unclear. Experimental animal models are valuable for exploring the etiologies and mechanisms of diseases and their interventions. In this review, we summarize how to establish a standardized rat model of asphyxia-induced cardiac arrest. There are four key focal areas: (1) selection of animal species; (2) factors to consider during modeling; (3) intervention management after return of spontaneous circulation; and (4) evaluation of neurologic function. The aim was to simplify a complex animal model, toward clarifying cardiac arrest pathophysiological processes. It also aimed to help standardize model establishment, toward facilitating experiment homogenization, convenient interexperimental comparisons, and translation of experimental results to clinical application.

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TGF-β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats

Yin

Wang

et al. 2019

Neurochem Res

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Emulsified isoflurane postconditioning improves survival and neurological outcomes in a rat model of cardiac arrest

Cited by 6 publications

References 39 publications

Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke

Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke

Rat model of asphyxia-induced cardiac arrest and resuscitation

TGF-β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats

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