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

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Abstract

Background

Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q ₁₀(CoQ ₁₀), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ ₁₀in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ ₁₀administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out.

Results

In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group ( p < 0.05). Administration of CoQ ₁₀after trauma was shown to be protective because it significantly lowered the increased MDA levels ( p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ ₁₀group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ ₁₀and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema ( p < 0.05).

Conclusion

Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ ₁₀use in rats with traumatic brain injury.

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Author and article information

Journal

Journal ID (nlm-ta): BMC Neurosci

Title: BMC Neuroscience

Publisher: BioMed Central

ISSN (Electronic): 1471-2202

Publication date Collection: 2011

Publication date (Electronic): 29 July 2011

Volume: 12

Page: 75

Affiliations

[1 ]Department of Neurosurgery, Faculty of Medicine, Zonguldak Karaelmas University, 67600, Kozlu, Zonguldak/TURKEY

[2 ]Department of Biochemistry, Faculty of Medicine, Zonguldak Karaelmas University, 67600, Kozlu, Zonguldak/TURKEY

[3 ]Deparment of Pathology, Faculty of Medicine, Zonguldak Karaelmas University, 67600, Kozlu, Zonguldak/TURKEY

[4 ]Department of Anesthesiology; Faculty of Medicine, Zonguldak Karaelmas University, 67600, Kozlu, Zonguldak/TURKEY

Article

Publisher ID: 1471-2202-12-75

DOI: 10.1186/1471-2202-12-75

PMC ID: 3160960

PubMed ID: 21801363

SO-VID: e9bec142-1eb9-49a5-b9eb-7f62a9920e5f

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.