Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Imaizumi, Yoichi; Mizushima, Hidekatsu; Matsumoto, Hiroaki; Dohi, Kenji; Matsumoto, Kiyoshi; Ohtaki, Hirokazu; Funahashi, Hiroomi; Matsunaga, Seiji; Horai, Reiko; Asano, Masahide; Iwakura, Yoichiro; Shioda, Seiji

doi:10.1267/ahc.34.357

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…Expression of NeuN and cleaved caspase-3 was detected by immunohistochemical staining, based on reported methods with some changes [9,25]. Brain sections were incubated with primary antibodies for NeuN (1:400, Cell Signaling) and cleaved caspase-3 (1:400, Cell Signaling) for 2 hr after blocking with 5% goat serum (Vector Labs, Burlingame, CA), and then incubated with secondary antibodies (DAKO, Glostrup, Denmark) at 37°C for 1 hr.…”

Section: Neuronal Apoptosismentioning

confidence: 99%

Retraction: Dexmedetomidine and Phosphocreatine Post-treatment Provides Protection against Focal Cerebral Ischemia-reperfusion Injury in Rats

Sun

Kang

Shen

et al. 2021

Acta Histochem. Cytochem

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In this study we investigated the neuroprotective efficacy of dexmedetomidine (Dex) and phosphocreatine (PCr) alone or in combination in a rat model of focal cerebral ischemiareperfusion injury (I/R). I/R was induced by intraluminal middle cerebral artery occlusion (MCAO) and reperfusion. Male Sprague-Dawley rats were randomly allocated to the Sham group and I/R group, and the I/R group was further divided into three subgroups: Dex (9 μg.kg −1 Dex), PCr (180 mg.kg −1 PCr) and Dex + PCr (9 μg.kg −1 Dex + 180 mg.kg −1 PCr). All treatments were given intravenously at the onset of reperfusion. After 24 hr of reperfusion, the neurological deficit score (NDS) was determined and a magnetic resonance imaging (MRI) scan was performed. Serum concentrations of malonaldehyde (MDA) and 4-hydroxynonenal (4-HNE) were measured and cerebral infarct volume was estimated by triphenyl tetrazolium chloride (TTC) staining. Blood brain barrier, neuronal and mitochondrial damage was assessed by optical and electron microscopy. Neuronal injury was further assessed using double cleaved caspase-3 and NeuN immunofluorescent staining. Compared with group I/R, Dex and PCr significantly reduced the neurological deficit score (P < 0.01), infarct volume (P < 0.01), and brain blood barrier, neuronal and mitochondrial damage. The level of oxidative stress (P < 0.001) and neuronal injury (P < 0.001) also decreased and surviving neurons increased (P < 0.001). Compared with Dex or PCr alone, the combination treatment had overall greater effects (P < 0.05). These results indicate that posttreatment with Dex or PCr decreases focal cerebral I/R injury and that these agents in combination have greater protective effects than each alone.

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Section: Neuronal Apoptosismentioning

confidence: 99%

Retraction: Dexmedetomidine and Phosphocreatine Post-treatment Provides Protection against Focal Cerebral Ischemia-reperfusion Injury in Rats

Sun

Kang

Shen

et al. 2021

Acta Histochem. Cytochem

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“…The expressions of IL-1b were noted several hours after ischemia and the proteins were strongest in the perifocal area at 24 h after tMCAO. Previous reports have suggested the involvement of endothelial cells, microglia, macrophages and astrocytes after ischemic and excitotoxic damage (Zhang et al, 1998;Hillhouse et al, 1998;Davies et al, 1999;Pearson et al, 1999;Imaizumi et al, 2001). However, in this study, the expression cells of IL-1b were only colocalized with microglia/macrophages, but not in astroglia and neuronal cells.…”

Section: Discussioncontrasting

confidence: 86%

Suppression of oxidative neuronal damage after transient middle cerebral artery occlusion in mice lacking interleukin-1

Ohtaki¹

2003

Neuroscience Research

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Interleukin-1 (IL-1) contributes to ischemic neurodegeneration. However, the mechanisms regulating action of IL-1 are still poorly understood. In order to clear this central issue, mice that were gene deficient in IL-1a and b (IL-1 KO) and wild-type mice were subjected to 1-h transient middle cerebral artery occlusion (tMCAO). Expression levels of IL-1b and IL-1 receptor I (IL-1RI) were then examined. Generation of peroxynitrite and the expression of mRNAs for nitric oxide synthase (NOS) subtypes were also determined. Immunostaining for IL-1b was increased from 6 h and peaked at 24 h after tMCAO in the microglia and macrophage. The immunoreactivities of IL-1RI were increased progressively in the microvasculature and neuron-like cells of the ipsilateral hemisphere. Infarct volumes were significantly lower in IL-1 KO mice compared with wild-type mice 48 h after tMCAO (P B/0.01). The immunoreactivities of 3-nitro-L-tyrosine were determined in the neurons and microvasculature 24 h after tMCAO and were significantly decreased in the IL-1 KO mice compared to wild-type mice. In addition, expression levels of NOS mRNA in IL-1 KO mice were lower than that measured in wild-type mice. These results indicate that IL-1 is up-regulated and may play a role in neurodegeneration by peroxynitrite production during ischemia. #

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“…Many endogenous angiogenic cytokines and growth factors such as vascular endothelial growth factor (VEGF) [14], fibroblast growth factor (FGF) [2], platelet derived growth factor (PDGF) [7], and interleukin-1b [8] have been reported to be expressed in ischemic neuronal death. Such substances, especially FGF, PDGF, transforming growth factor-b (TGFb), epidermal growth factor (EGF), and thrombin, were demonstrated to promote leptomeningeal cell proliferation in culture [16].…”

Section: Resultsmentioning

confidence: 99%

Proliferation of Leptomeningeal Cells in Delayed Neuronal Death in Gerbils

Kataoka

Cui

Tamura

et al. 2004

Acta Histochem. Cytochem

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Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Cited by 8 publications

References 24 publications

Retraction: Dexmedetomidine and Phosphocreatine Post-treatment Provides Protection against Focal Cerebral Ischemia-reperfusion Injury in Rats

Retraction: Dexmedetomidine and Phosphocreatine Post-treatment Provides Protection against Focal Cerebral Ischemia-reperfusion Injury in Rats

Suppression of oxidative neuronal damage after transient middle cerebral artery occlusion in mice lacking interleukin-1

Proliferation of Leptomeningeal Cells in Delayed Neuronal Death in Gerbils

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