Background And Aim: Traumatic brain injury (TBI) results in death or long term functional disabilities. Eugenol is demonstrated to be beneficial in a range of experimental models of neurological disorders via its anti-inflammatory and antioxidant properties. Thus, the present study was designed to investigate the neuroprotective effects of eugenol in a weight-drop induced rat model of TBI.
Experimental Procedure: Rats were assigned into five groups; control and TBI groups pretreated with vehicle, and three TBI groups pretreated with different doses of eugenol (25, 50, and 100 mg/kg/day, , seven consecutive days). Except for the control, all other groups were subjected to TBI using Marmarou's weight-drop method. 24 h after TBI, locomotor functions and short term memory were evaluated. Lastly animals were scarified and the estimation of lipid peroxidation in brain tissue, blood-brain barrier (BBB) integrity, brain water content (brain edema) and histopathology of the brain tissue were performed.
Results: Weight-drop induced TBI caused functional disabilities in the rats as indicated by impairment in locomotor activities and short term memory. The TBI also resulted in augmented neuronal cell death designated by chromatolysis. The results also showed disruption in the BBB integrity, increased edema, and lipid peroxidation in the brain of the rats exposed to trauma. Pretreatment with eugenol (100 mg/kg) ameliorated histopathological, neurochemical, and behavioral consequences of trauma.
Conclusion: For the first time this study revealed that eugenol can be considered as a potential candidate for managing the functional disabilities associated with TBI because of its antioxidant activities.
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http://dx.doi.org/10.1016/j.jtcme.2021.01.003 | DOI Listing |
Australas J Ageing
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School of Nursing, Centre for Healthcare Transformation, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia.
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Private Practice, Zubná Pohotovosť, s.r.o. Bratislava, Krížna 44, Slovakia.
Our review study addresses the issue of tooth loss, which is caused by loss of masticatory function and its impact on cognitive functions, dementia, and Alzheimer's disease. Numerous studies have confirmed a positive correlation between premature tooth loss, reduction in masticatory function and significant cognitive decline observed through learning disabilities, including overcoming ordinary life problems to early and advanced forms of dementia. Reduced numbers of teeth in the main food processing area, i.
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