Difference of fibroblast growth factor receptor 1 expression among CA1-3 regions of the gerbil hippocampus after transient cerebral ischemia

Yoo, Ki‐Yeon; Hwang, In Koo; Lee, Choong Hyun; Choi, Jung Hoon; Kwon, Seung‐Hae; Kang, Il‐Jun; You, Sung Hyun; Kim, Young‐Myeong; Won, Moo‐Ho

doi:10.1016/j.jns.2010.06.018

Cited by 3 publications

(1 citation statement)

References 30 publications

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“…On the contrary, VEGFR1 negatively regulates cell proliferation and reduces angiogenesis ( Mendes et al, 2018 ). Increasing evidence suggests that cerebral ischemia upregulates VEGFR1 expression, which positively correlates with the degree of damage ( Yoo et al, 2010 ; Causey et al, 2012 ). In a BMECs model treated with OGD, borneol increased the expression of VEGF, reduced the expression of VEGFR1, and tended to increase the expression of VEGFR2 ( Yu et al, 2019a ).…”

Section: Resultsmentioning

confidence: 99%

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Ren

Wang

et al. 2021

Front. Pharmacol.

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Background: Borneol is a terpene and bicyclic organic compound that can be extracted from plants or chemically synthesized. As an important component of proprietary Chinese medicine for the treatment of stroke, its neuroprotective effects have been confirmed in many experiments. Unfortunately, there is no systematic review of these studies. This study aimed to systematically examine the neuroprotective effects of borneol in the cascade reaction of experimental ischemic stroke at different periods.Methods: Articles on animal experiments and cell-based research on the actions of borneol against ischemic stroke in the past 20°years were collected from Google Scholar, Web of Science, PubMed, ScienceDirect, China National Knowledge Infrastructure (CNKI), and other biomedical databases. Meta-analysis was performed on key indicators in vivo experiments. After sorting the articles, we focused on the neuroprotective effects and mechanism of action of borneol at different stages of cerebral ischemia.Results: Borneol is effective in the prevention and treatment of nerve injury in ischemic stroke. Its mechanisms of action include improvement of cerebral blood flow, inhibition of neuronal excitotoxicity, blocking of Ca2+ overload, and resistance to reactive oxygen species injury in the acute ischemic stage. In the subacute ischemic stage, borneol may antagonize blood-brain barrier injury, intervene in inflammatory reactions, and prevent neuron excessive death. In the late stage, borneol promotes neurogenesis and angiogenesis in the treatment of ischemic stroke.Conclusion: Borneol prevents neuronal injury after cerebral ischemia via multiple action mechanisms, and it can mobilize endogenous nutritional factors to hasten repair and regeneration of brain tissue. Because the neuroprotective effects of borneol are mediated by various therapeutic factors, deficiency caused by a single-target drug is avoided. Besides, borneol promotes other drugs to pass through the blood-brain barrier to exert synergistic therapeutic effects.

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Section: Resultsmentioning

confidence: 99%

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Ren

Wang

et al. 2021

Front. Pharmacol.

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The Effect of Repeated Resveratrol Administration on Global Ischemia-Induced Hippocampal Neurodegeneration, Neurochemical Effects and Functional Alterations

Girbovan¹

2015

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Effects of Transient Forebrain Ischemia on the Hippocampus of the Mongolian Gerbil (Meriones unguiculatus): An Immunohistochemical Study

et al. 2013

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In the Mongolian gerbil, bilateral common carotid artery occlusion (BCCAO) for several minutes induces ischemia and delayed neuronal cell death in the CA1 region of the hippocampus due to their incomplete Circle of Willis. In the present study, the expression of fibroblast growth factor 2 (FGF2), its receptors (FGFR1 and FGFR2), glial fibrillary acidic protein (GFAP), and isolectin B4 (ISLB4) was investigated by immunohistochemical and lectin-binding methods after BCCAO was performed for 5 min in gerbils. One day after BCCAO, the pyramidal cells of the CA1 region of the hippocampus showed degenerative changes and lowered expression of FGF2, FGFR1, and FGFR2. Three days after BCCAO, there was an increase in GFAP-positive astrocytes and ISLB4-positive microglial cells. From five to 10 days after BCCAO, intense neuronal cell death in the stria pyramidale of the hippocampal CA1 region was observed, as well as an increase in GFAP-positive astrocytes and decrease in ISLB4-positive microglial cells. These results indicate that transient forebrain ischemia induces neuronal cell death with lowered expression of FGF2 and its receptors, and that the activation of glial cells may not directly lead to neuronal cell death.

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Difference of fibroblast growth factor receptor 1 expression among CA1-3 regions of the gerbil hippocampus after transient cerebral ischemia

Cited by 3 publications

References 30 publications

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

The Effect of Repeated Resveratrol Administration on Global Ischemia-Induced Hippocampal Neurodegeneration, Neurochemical Effects and Functional Alterations

Effects of Transient Forebrain Ischemia on the Hippocampus of the Mongolian Gerbil (Meriones unguiculatus): An Immunohistochemical Study

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