Experimental study on the protective effects of edaravone against ischemic spinal cord injury

Suzuki, Kazunao; Kazui, Teruhisa; Terada, Hitoshi; Umemura, Kazuo; Ikeda, Yasuhiko; Bashar, Abul Hasan Muhammad; Yamashita, Katsushi; Washiyama, Naoki; Suzuki, Takahiro; Ohkura, Kazuhiro; Yasuike, Junji

doi:10.1016/j.jtcvs.2005.08.049

Cited by 41 publications

(32 citation statements)

References 26 publications

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“…In addition, Eda not only had antioxidant roles, but also protected cells from apoptosis [16,17] . However, little information is available on antioxidant Eda in regulating the Bcl-2/Bax apoptotic pathway via mitochondria after CoCl 2 injury at cellular level.…”

Section: Discussionmentioning

confidence: 97%

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

2009

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Objective To investigate the neuroprotective effects of edaravone (Eda) on cobalt chloride (CoCl 2 )-induced oxidative stress and apoptosis in cultured PC12 cells as well as the underlying mechanisms. Methods PC12 cells impaired by CoCl 2 were used as the cell model of hypoxia. MTT (methyl thiazolyl tetrazolium) was used to assay the viability of the PC12 cells exposed to Eda with gradient concentrations; Hochest 33258 stain assay was used to analyze the apoptosis ratio of the PC12 cells; Bcl-2 and Bax protein levels in PC12 cells were examined by western blotting. ROS level, the mitochondrial transmembrane potential and caspase-3 activity in each group were detected by spectrofluorometer. Results CoCl 2 treatment caused the loss of cell viability in PC12 cells, which was associated with the elevation of apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. CoCl 2 also significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, Eda significantly reversed these phenotypes, with its maximum protective effect at 0.1 μmol/L. Conclusion These results indicated that Eda could protect PC12 cells from CoCl 2 -induced cytotoxicity, and this protection might be ascribed to its anti-oxidative and anti-apoptotic activities.

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Section: Discussionmentioning

confidence: 97%

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

2009

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“…A previous study showed that edaravone could decrease calcium overloading, increase mitochondrial potential, and reduce neuronal apoptosis through inhibiting lipid peroxidation in the rat hippocampal I/R model [15] . Wen et al reported that edaravone could relieve oxidative stress through inhibiting the JNK-c-Jun pathway in the senile rat cerebral I/R model and therefore protect cerebral neurons [14] . The present study has indicated the involvement of antioxidative and antiapoptotic effects of edaravone on photoreceptor cells in the rat retinal I/R model, but whether these 2 pathways also apply to the retinal I/R injury model warrants further study.…”

Section: Discussionmentioning

confidence: 99%

Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemiareperfusion injury in rats¹

Song

Gong

Xie

et al. 2008

Acta Pharmacologica Sinica

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Aim: To investigate the effect of edaravone (MCI-186), a free radical scavenger, against ischemia/reperfusion (I/R) injury in the rat retina. Methods: Retinal ischemia was induced in male Sprague-Dawley rats by elevating intraocular pressure to 110 mmHg for 60 min. The rats were intraperitoneally injected with edaravone at a dose of 3 mg/kg at 30 min before ischemia, and then treated with edaravone (3 mg/kg, ip) twice daily for 1 or 5 d after I/R. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the retinal tissues were determined on d 1 after I/R injury. The apoptosis of retinal neurons was detected on d 1 after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. The electroretinogram (ERG) was recorded on d 5 after reperfusion. Results: Edaravone lowered MDA levels, raised SOD activity, and attenuated I/R-induced apoptosis of retinal neurons within the inner nuclear, ganglion cell, and outer nuclear layers of the rat retina. Moreover, edaravone suppressed I/R-induced reduction in a-and b-wave amplitudes of ERG. Conclusion: Edaravone can protect the retina from I/R injury in rats through reducing oxidative stress and inhibiting apoptosis of retinal neurons, which suggests that edaravone might be a potential choice for the treatment of I/R-induced eye disorders.

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“…Using a rat model of transient middle cerebral artery occlusion (MCAO), the data showed that daily treatment with edaravone reduced cortical infarction volume. In addition, edaravone not only has antioxident action, but also protects cells from apoptosis (Kokura et al, 2005;Suzuki et al, 2005). However, little information is available on antioxidant edaravone in regulating the Bcl-2/Bax apoptotic pathway via mitochondria after OGD-reperfusion injury at cellular level.…”

Section: Introductionmentioning

confidence: 99%

Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria

Song¹,

Li²,

Li³

et al. 2006

J. Zhejiang Univ. - Sci. B

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Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation)-reperfusion. Methods: Viability of PC12 cells which were injured at different time of OGD injury, was quantified by measuring MTT (2-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) staining. In addition, PC12 cells' viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by (OGD). Furthermore, apoptotic population of PC12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/PI staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot. Results: (1) The viability of PC12 cells decreased with time (1~12 h) after OGD. We regarded the model of OGD 2 h, then replacing DMEM (Dulbecco's Modified Eagle's Medium) for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 µmol/L) increased significantly with edaravone protecting PC12 cells from apoptosis after OGD-reperfusion injury. (3) Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion. Conclusion: Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria.

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Experimental study on the protective effects of edaravone against ischemic spinal cord injury

Abstract: Edaravone exerted a significant protective effect on the spinal cord against ischemia-reperfusion injury by suppressing the level of free radical species, which was demonstrated with the microdialysis method.

Cited by 41 publications

References 26 publications

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemiareperfusion injury in rats¹

Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria

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Experimental study on the protective effects of edaravone against ischemic spinal cord injury

Abstract: Edaravone exerted a significant protective effect on the spinal cord against ischemia-reperfusion injury by suppressing the level of free radical species, which was demonstrated with the microdialysis method.

Cited by 41 publications

References 26 publications

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemiareperfusion injury in rats1

Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria

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Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemiareperfusion injury in rats¹