α7 Nicotinic acetylcholine receptor agonist attenuates neuropathological changes associated with intracerebral hemorrhage in mice

Hijioka, Masanori; Matsushita, Hideaki; Ishibashi, Hayato; Hisatsune, Akinori; Isohama, Yoichiro; Katsuki, Hiroshi

doi:10.1016/j.neuroscience.2012.07.024

Cited by 39 publications

(32 citation statements)

References 34 publications

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“…In addition, the nicotine treated mice showed improved sensorimotor performance assessed on beam-walking, modified limb-placing and adhesive removal test with improved overall survival rate (Hijioka et al 2011). Similar effects are seen with ICH mice treated with a direct α7 nAChR agonist (Hijioka et al 2012). …”

Section: Introductionsupporting

confidence: 63%

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Kathirvelu

Carmichael

2014

Metab Brain Dis

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There has been strong pre-clinical research on mechanisms of initial cell death and tissue injury in intracerebral hemorrhage (ICH). This data has led to the evaluation of several therapeutics for neuroprotection or the mitigation of early tissue damage. Most of these studies have been done in the rat. Also, there has been little study of the mechanisms of tissue repair and recovery. This review examines the testing of candidate therapeutics in mouse models of ICH for their effect on tissue protection and repair. This review will help the readers compare it to the extensively researched rat model of ICH and thus enhance work that are pending in mouse model.

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Section: Introductionsupporting

confidence: 63%

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Kathirvelu

Carmichael

2014

Metab Brain Dis

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“…In a similar series of experiments, Hijioka et al 15 demonstrated an increase in the number of surviving neurons and an attenuation of the inflammatory cell infiltrate in the perihematomal region, but no significant effect on BWC (functional outcome was not assessed in this study). This lack of effect on BWC is in contrast to the findings of Krafft et al, as described above.…”

Section: Results Of α7 Stimulation In Experimental Ichmentioning

confidence: 42%

Alpha-7 nicotinic acetylcholine receptor agonists in intracerebral hemorrhage: an evaluation of the current evidence for a novel therapeutic agent

Sussman¹,

Kellner²,

McDowell³

et al. 2013

FOC

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Intracerebral hemorrhage (ICH) is the most deadly and least treatable subtype of stroke, and at the present time there are no evidence-based therapeutic interventions for patients with this disease. Secondary injury mechanisms are known to cause substantial rates of morbidity and mortality following ICH, and the inflammatory cascade is a major contributor to this post-ICH secondary injury. The alpha-7 nicotinic acetylcholine receptor (α7-nAChR) agonists have a well-established antiinflammatory effect and have been shown to attenuate perihematomal edema volume and to improve functional outcome in experimental ICH. The authors evaluate the current evidence for the use of an α7-nAChR agonist as a novel therapeutic agent in patients with ICH.

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“…Construction of ICH mouse models were performed according to a previously published protocol [14]. Briefly, male C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME, USA) of 20–22 months were used to produce ICH models with collagenase-induction method.…”

Section: Methodsmentioning

confidence: 99%

Fisetin Protects against Intracerebral Hemorrhage-Induced Neuroinflammation in Aged Mice

et al. 2018

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Background: Fisetin is commonly used as an anti-inflammatory and neuroprotective drug. In this study, we aimed to investigate the efficacy of fisetin in alleviating intracerebral hemorrhage (ICH)-induced brain injury. Methods: Mouse ICH models were constructed using the collagenase-induction method. ICH mice received fisetin treatment at the dose of 10–90 mg/kg, followed by the evaluation of neurological deficit through neurologic severity scores (mNSS), brain water content and terminal deoxynucleotidyl transferase dUTP nick end labeling analysis of cell apoptosis. Cytokine levels were also assessed with enzyme-linked immunosorbent assay. The activation of astrocytes and microglia was evaluated through S100 staining and Western blot analysis of ionized calcium-binding adaptor molecule 1 respectively. Nuclear factor kappa-B (NF-κB) signaling was also evaluated by Western blot. Results: ICH mice demonstrated dramatic increase in mNSS, brain edema and cell apoptosis, indicating severe brain deficit. Fisetin treatment lowered these parameters, suggesting the alleviation of brain injury. Levels of proinflammatory cytokines were reduced, accompanied by a prominent decrease in activated astrocytes and microglia. NF-κB signaling was also attenuated by fisetin treatment. Conclusion: Fisetin effectively alleviates ICH by downregulating proinflammatory cytokines and attenuating NF-κB signaling. These data suggest fisetin as a valuable natural flavonol for clinical management of ICH-induced brain injury.

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α7 Nicotinic acetylcholine receptor agonist attenuates neuropathological changes associated with intracerebral hemorrhage in mice

Cited by 39 publications

References 34 publications

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Alpha-7 nicotinic acetylcholine receptor agonists in intracerebral hemorrhage: an evaluation of the current evidence for a novel therapeutic agent

Fisetin Protects against Intracerebral Hemorrhage-Induced Neuroinflammation in Aged Mice

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