Mitochondrial Targeted Antioxidant in Cerebral Ischemia

Ahmed, Ejaz; Tucker, Donovan; Lu, Yujiao; Zhang, Quanguang

doi:10.21767/2171-6625.100017

Cited by 31 publications

(20 citation statements)

References 66 publications

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“…Coenzyme Q10 (CoQ10) is a mitochondrial targeted antioxidant that plays an essential role in the normal function of the electron transport chain. CoQ10 has been reported to exhibit neuroprotective activity in a range of disorders including; cerebral ischemia, ( Ahmed et al, 2015 ) Parkinson's disease and Huntington's disease ( Klongpanichapak et al, 2006 ). In addition to its role as an antioxidant, CoQ10 is also reported to protect against glutamate excitotoxicity in vivo through the inhibition of mitochondrial depolarization ( Papucci et al, 2003 , Lee et al, 2014b ).…”

Section: Introductionmentioning

confidence: 99%

Topical Coenzyme Q10 demonstrates mitochondrial-mediated neuroprotection in a rodent model of ocular hypertension

Davis¹,

Tian²,

Pahlitzsch³

et al. 2017

Mitochondrion

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Coenzyme Q10 (CoQ10) is a mitochondrial-targeted antioxidant with known neuroprotective activity. Its ocular effects when co-solubilised with α–tocopherol polyethylene glycol succinate (TPGS) were evaluated. In vitro studies confirmed that CoQ10 was significantly protective in different retinal ganglion cell (RGC) models. In vivo studies in Adult Dark Agouti (DA) rats with unilateral surgically-induced ocular hypertension (OHT) treated with either CoQ10/TPGS micelles or TPGS vehicle twice daily for three weeks were performed, following which retinal cell health was assessed in vivo using DARC (Detection of Apoptotic Retinal Cells) and post-mortem with Brn3a histological assessment on whole retinal mounts. CoQ10/TPGS showed a significant neuroprotective effect compared to control with DARC (p < 0.05) and Brn3 (p < 0.01). Topical CoQ10 appears an effective therapy preventing RGC apoptosis and loss in glaucoma-related models.

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Section: Introductionmentioning

confidence: 99%

Topical Coenzyme Q10 demonstrates mitochondrial-mediated neuroprotection in a rodent model of ocular hypertension

Davis¹,

Tian²,

Pahlitzsch³

et al. 2017

Mitochondrion

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“…Under normal circumstances, there is a balance between ROS generation and the endogenous antioxidant systems in the cell. However, ischemia and reperfusion disturb the balance of the endogenous antioxidant system, which increases oxidative stress by the overproduction of cellular ROS and ultimately leads to neuronal death 19–21. SOD, CAT and GSH-PX, as the endogenous antioxidant enzymes, are believed to play vital roles in the defense mechanisms against free radical-induced oxidative stress 22,23.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of curdione against focal cerebral ischemia reperfusion injury in rats

Li¹,

Li²,

Shi³

et al. 2017

NDT

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BackgroundCurdione is one of the most highly concentrated component of the active constituents in E-zhu, which has been reported to possess a variety of activities. However, the pharmacologic neuroprotective activity of curdione has not been evaluated. The present study aimed to investigate the protective effect of curdione on focal cerebral ischemia reperfusion-induced injury in rats and further exploring the underlying mechanisms.Materials and methodsAdult male Sprague Dawley rats were subjected to middle cerebral artery occlusion (MCAO) surgery for 2 h, followed by reperfusion stage. All animals received treatment once a day for 7 days before surgery and 14 days from 4 h after the reperfusion started. The neurological deficit test and Morris water maze test were performed at 1, 4, 7 and 14 days after MCAO. The infarct size of animals was determined by the 2,3,5-triphenyltetrazolium chloride staining, and pathological brain damage was estimated by hematoxylin–eosin staining. The malonaldehyde (MDA) levels and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) were detected by enzyme-linked immunosorbent assay. Expression of apoptotic proteins was measured by Western blot.ResultsOur results showed that curdione could significantly reduce the infarct size and neurological deficits, promote cognitive function recovery and recover neuronal morphologic damages in MCAO rats. It also blocked the increase of MDA content and elevated the activities of SOD, CAT and GSH-PX. Moreover, curdione attenuated the expression of Cyt-C, c-caspase-3 and c-caspase-9 increased the Bcl-2/Bax ratio and hence decreased the cellular apoptosis.ConclusionCurdione possessed potential neuroprotective effect on rats in the MCAO model. The anti-oxidative and anti-apoptotic properties may be involved in the underlying mechanisms.

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“…Coenzyme Q10 (CoQ10) is a mitochondrial targeted antioxidant that plays an essential role in the normal function of the electron transport chain. CoQ10 has been reported to have neuroprotective activity in neurodegenerative diseases and cerebral ischemia [81]. In addition to its antioxidant function, CoQ10 is also reported to protect against glutamate excitotoxicity [82].…”

Section: Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

Current Medical Therapy and Future Trends in the Management of Glaucoma Treatment

Cvenkel

Kolko

2020

Journal of Ophthalmology

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Glaucoma is a neurodegenerative disease characterized by progressive loss of retinal ganglion cells and their axons. Lowering of intraocular pressure (IOP) is currently the only proven treatment strategy for glaucoma. However, some patients show progressive loss of visual field and quality of life despite controlled IOP which indicates that other factors are implicated in glaucoma. Therefore, approaches that could prevent or decrease the rate of progression and do not rely on IOP lowering have gained much attention. Effective neuroprotection has been reported in animal models of glaucoma, but till now, no neuroprotective agents have been clinically approved. The present update provides an overview of currently available IOP-lowering medications. Moreover, potential new treatment targets for IOP-lowering and neuroprotective therapy are discussed. Finally, future trends in glaucoma therapy are addressed, including sustained drug delivery systems and progress toward personalized medicine.

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Mitochondrial Targeted Antioxidant in Cerebral Ischemia

Cited by 31 publications

References 66 publications

Topical Coenzyme Q10 demonstrates mitochondrial-mediated neuroprotection in a rodent model of ocular hypertension

Topical Coenzyme Q10 demonstrates mitochondrial-mediated neuroprotection in a rodent model of ocular hypertension

Neuroprotective effects of curdione against focal cerebral ischemia reperfusion injury in rats

Current Medical Therapy and Future Trends in the Management of Glaucoma Treatment

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