Neuroprotection of Oral Edaravone on Middle Cerebral Artery Occlusion in Rats

Zhao, Liqin; Parikh, Ankit; Xiong, Ye; Ye, Qing-Yan; Yingguo,; Zhou, Xin‐Fu; Hy, Luo

doi:10.1007/s12640-022-00520-8

Cited by 5 publications

(4 citation statements)

References 26 publications

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“…We have, however, used a daily dose of 40 mg/kg, which is much higher than that used in humans [67,68]. Furthermore, our dose was comparable or even slightly higher then oral dosage shown effective in a rat model of cerebral artery occlusion [69] or in a mouse model of the Alzheimer's disease [61]. Administration of edaravone suspension directly to the mouth of the mice allowed relatively good control over the drug intake.…”

Section: Discussionmentioning

confidence: 89%

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Sucha,

Benediktova,

Tichanek

et al. 2023

Preprint

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Edaravone is a mitochondrially targeted drug with a suggested capability to modify the course of diverse neurological diseases. Nevertheless, edaravone has not been tested yet in the context of spinocerebellar ataxia 1 (SCA1), an incurable neurodegenerative disease characterized mainly by cerebellar disorder with a strong contribution of inflammation and mitochondrial dysfunction. This study aimed to address this gap, exploring the potential of edaravone to slow down SCA1 progression in a mouse knock-in SCA1 model. SCA1154Q/2Q and healthy SCA12Q/2Q mice were getting either edaravone or saline daily for more than 13 weeks. The functional impairments were assessed via a wide spectrum of behavioral assays reflecting motor and cognitive deficits and behavioral abnormalities. Moreover, we used high-resolution respirometry to explore mitochondrial function, and immunohistochemical and biochemical tools to assess the magnitude of neurodegeneration, inflammation and neuroplasticity. Data were analyzed using (hierarchical) Bayesian regression models combined with the methods of multivariate statistics. Our analysis pointed out various previously documented neurological and behavioral deficits of SCA1 mice. However, we did not detect any plausible therapeutic effect of edaravone on either behavioral dysfunctions or other disease hallmarks in SCA1 mice. Thus, our results did not provide support for the therapeutic potential of edaravone in SCA1.

show abstract

Section: Discussionmentioning

confidence: 89%

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Sucha,

Benediktova,

Tichanek

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…However, we used a daily dose of 40 mg/kg, which is much higher than that used in humans [68,69]. Furthermore, our dose was comparable to, or even slightly higher than, the oral dosage shown as being effective in a rat model of cerebral artery occlusion [70] or in a mouse model of Alzheimer's disease [62]. Administration of edaravone suspension directly into the mouths of the mice allowed relatively good control over the drug intake.…”

Section: Discussionmentioning

confidence: 99%

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Sucha,

Benediktova,

Tichanek

et al. 2023

IJMS

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Edaravone is a mitochondrially targeted drug with a suggested capability to modify the course of diverse neurological diseases. Nevertheless, edaravone has not been tested yet in the context of spinocerebellar ataxia 1 (SCA1), an incurable neurodegenerative disease characterized mainly by cerebellar disorder, with a strong contribution of inflammation and mitochondrial dysfunction. This study aimed to address this gap, exploring the potential of edaravone to slow down SCA1 progression in a mouse knock-in SCA1 model. SCA1154Q/2Q and healthy SCA12Q/2Q mice were administered either edaravone or saline daily for more than 13 weeks. The functional impairments were assessed via a wide spectrum of behavioral assays reflecting motor and cognitive deficits and behavioral abnormalities. Moreover, we used high-resolution respirometry to explore mitochondrial function, and immunohistochemical and biochemical tools to assess the magnitude of neurodegeneration, inflammation, and neuroplasticity. Data were analyzed using (hierarchical) Bayesian regression models, combined with the methods of multivariate statistics. Our analysis pointed out various previously documented neurological and behavioral deficits of SCA1 mice. However, we did not detect any plausible therapeutic effect of edaravone on either behavioral dysfunctions or other disease hallmarks in SCA1 mice. Thus, our results did not provide support for the therapeutic potential of edaravone in SCA1.

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“…In terms of the study of molecular pathways, Hu et al [41] showed that edaravone dexborneol effectively suppressed nucleotide-binding oligomerization domain-like receptor pyrin domain-containing protein 3 (NLRP3) inflammation-induced activation of microglial pyroptosis in experimental ischemic stroke through NF-κB/ NLRP3/gasdermin D (GSDMD) signaling pathway using transient MCAO (tMCAO) mouse model in vivo and oxygen-glucose deprivation (OGD) BV2 cell model in vitro. A multi-center, randomized, double-blind, controlled phase III trial, Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia (TASTE) trial [42], enrolled 1,165 AIS patients who were randomly assigned to receive either edaravone dexborneol or edaravone. The proportion of patients with good functional outcomes at 90 days was significantly higher in the edaravone dexborneol group than in the edaravone group [mRS score ≤ 1, 67.18% vs. 58.97%; odds ratio (OR): 1.42; 95% confidence interval (CI): 1.12 to 1.81; P = 0.004].…”

Section: Edaravone Dexborneolmentioning

confidence: 99%

Advances in neuroprotective therapy for acute ischemic stroke

Yang,

Guo,

Liu

et al. 2024

Explor Neuroprot Ther

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Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is significant in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transformation after recanalization predict poor prognosis of AIS. How to minimize reperfusion injury and hemorrhagic transformation, which greatly improves the prognosis of vascular recanalization, is becoming a hot topic in AIS research and an urgent problem to be solved. A wealth of neuroprotective drug studies is now available, while some of the neuroprotectants have met with failure in human studies. It is discussed in this review about the progress in neuroprotective therapy for AIS based on understanding the pathophysiologic mechanisms of reperfusion injury and hemorrhagic transformation, as well as challenges in exploring new neuroprotectants.

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Neuroprotection of Oral Edaravone on Middle Cerebral Artery Occlusion in Rats

Cited by 5 publications

References 26 publications

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1

Advances in neuroprotective therapy for acute ischemic stroke

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