Effect of Coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats

Kalaycı, Murat; Unal, Mufit M; Gül, Şanser; Açıkgöz, Şerefden; Kandemır, Nilüfer Onak; Hancı, Volkan; Edebali, Nurullah; Açıkgöz, Bektaş

doi:10.1186/1471-2202-12-75

Cited by 58 publications

(39 citation statements)

References 30 publications

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“…6,23 Our findings, which demonstrated the decreased oxidative stress following CoQ 10 administration, agree with previous studies that used various cerebral injury models. 1,10,25 In an experimental traumatic brain injury model, the group treated with CoQ 10 after head trauma showed significantly lower MDA levels and attenuated neuronal damage compared with the control group. 10 In an animal model of temporal lobe epilepsy, CoQ 10 pretreatment effectively reduced the increase of kainate-induced intrahippocampal MDA level and attenuated hippocampal neuronal loss.…”

Section: Discussionmentioning

confidence: 99%

“…1,10,25 In an experimental traumatic brain injury model, the group treated with CoQ 10 after head trauma showed significantly lower MDA levels and attenuated neuronal damage compared with the control group. 10 In an animal model of temporal lobe epilepsy, CoQ 10 pretreatment effectively reduced the increase of kainate-induced intrahippocampal MDA level and attenuated hippocampal neuronal loss. 1 CoQ 10 supplementation also decreased the MDA level and attenuated beta-amyloid pathology in an Alzheimer disease model.…”

Section: Discussionmentioning

confidence: 99%

“…CoQ 10 may modulate several cellular processes associated with the neuroprotective effect against spinal cord ischemia-reperfusion injury. Further studies are required to determine the mechanisms of the neuroprotective effect of CoQ 10 .…”

Section: Discussionmentioning

confidence: 99%

“…13,17 The related mechanisms of the neuroprotective effect of CoQ 10 are modulation of oxidative stress and attenuation of apoptotic cell death. 20 The important role of oxidative stress in spinal cord ischemia-reperfusion injury suggests that CoQ 10 may have a protective effect, 22 but the effect of CoQ 10 on spinal cord ischemia has not been determined.…”

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confidence: 99%

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Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury

Hwang

Min

Jeon

et al. 2015

SPI

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OBJECT Spinal cord ischemia remains a serious complication of thoracoabdominal aortic aneurysm surgery. Coenzyme Q10, a potent antioxidant, has been reported to exert a neuroprotective effect. In the present study, we evaluated the effect of coenzyme Q10 pretreatment on spinal cord ischemia-reperfusion injury. METHODS Male Sprague-Dawley rats were treated with either 300 mg/kg coenzyme Q10 (CoQ10 group, n = 12) or saline (control and sham groups, n = 12 for each group) for 5 days before ischemia. Spinal cord ischemia was induced in the control and CoQ10 groups. Neurological function was assessed using the Basso-Beattie-Bresnahan (BBB) motor rating scale until 7 days after reperfusion, and then the spinal cord was harvested for histopathological examinations and an evaluation of malondialdehyde level. RESULTS On post-reperfusion Day 1, the CoQ10 group showed higher BBB scores compared with those in the control group, although the difference was not significant. However, on Day 2, the CoQ10 group showed a significantly higher BBB score than the control group (14.0 [10.3–15.0] vs 8.0 [5.0–9.8], median [IQR], respectively; p = 0.021), and this trend was maintained until Day 7 (17.5 [16.0–18.0] vs 9.0 [6.5–12.8], respectively; p < 0.001). Compared with the control group, the CoQ10 group had more normal motor neurons (p = 0.003), fewer apoptotic changes (p = 0.003) and a lower level of tissue malondialdehyde (p = 0.024). CONCLUSIONS Pretreatment with 300 mg/kg coenzyme Q10 resulted in significantly improved neurological function and preservation of more normal motor neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury

Hwang

Min

Jeon

et al. 2015

SPI

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“…The examination of the histological changes consisted of evaluating the following parameters: vascular congestion, intraparenchymal hemorrhage, inflammation, edema and gliosis. The examination of the neuronal degenerative changes consisted of the evaluation of the following: nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal swelling (1,7,19,23,29,30,44,53).…”

Section: Histological Examinationsmentioning

confidence: 99%

Effectiveness of gfap in determining neuron damage in rats with induced head trauma

Çıkrıklar¹,

Uysal²,

Ekici³

et al. 2015

Turkish Neurosurgery

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spread neurodegeneration and is still a major worldwide health problem (2,33,44,50,51). TBI causes not only direct mechanical damage to the brain, but it also induces biochemical changes that lead to delayed neural cell loss. These biochemical changes are called secondary injury. The primary █ INTRODUCTION O ne common form of acute brain injury, traumatic brain injury (TBI), is the result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events that collectively mediate wideAIm: To determine whether the serum level of glial fibrillary acidic protein (GFAP), an important indicator of neuron damage, correlates with the extent of tissue damage in the rat with induced head trauma and to obtain data in order to avoid unnecessary cranial computed tomography analyses. mATERIAl and mEThODS: Three-month-old male Sprague-Dawley rats were used. Rats were divided into 5 groups. The experimental head trauma model was examined in five groups (n=8) as follows: The control group had no intervention; Group 1: Head trauma was induced by dropping a 25 mg ball from a height of 20 cm; Group 2: Head trauma was induced by dropping a 50 mg ball from a height of 20 cm; Group 3: Head trauma was induced by dropping a 50 mg ball from a height of 80 cm; Group 4: Head trauma was induced by dropping a 100 mg ball from a height of 80 cm. Thus, according to the Newton's Law, respectively 0.05, 0.1, 0.2 and 0.4 N trauma was created. Serum GFAP levels were analyzed and the damage to cerebral tissues was evaluated in all groups. RESUlTS:We determined that number of apoptotic cells and particularly the number of GFAP (+) protoplasmic astrocytes at the perilesional region of the cortex increased in association with the increased serum GFAP level as long as the severity of the trauma increased.CONClUSION: Serum GFAP concentration can be used as a marker of the severity of head trauma and traumatic brain injury. However, more animal studies are required to reflect this result in clinical practice.

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Mitochondrial dynamics, mitophagy and biogenesis in neonatal hypoxic‐ischaemic brain injury

et al. 2017

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Hypoxic-ischaemic encephalopathy, resulting from asphyxia during birth, affects 2-3 in every 1000 term infants and depending on severity, brings about life-changing neurological consequences or death. This hypoxic-ischaemia (HI) results in a delayed neural energy failure during which the majority of brain injury occurs. Currently, there are limited treatment options and additional therapies are urgently required. Mitochondrial dysfunction acts as a focal point in injury development in the immature brain. Not only do mitochondria become permeabilised, but recent findings implicate perturbations in mitochondrial dynamics (fission, fusion), mitophagy and biogenesis. Mitoprotective therapies may therefore offer a new avenue of intervention for babies who suffer lifelong disabilities due to birth asphyxia.

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Effect of Coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats

Cited by 58 publications

References 30 publications

Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury

Effect of coenzyme Q10 on spinal cord ischemia-reperfusion injury

Effectiveness of gfap in determining neuron damage in rats with induced head trauma

Mitochondrial dynamics, mitophagy and biogenesis in neonatal hypoxic‐ischaemic brain injury

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