Clinical and Basic Evaluation of the Prognostic Value of Uric Acid in Traumatic Brain Injury
| Autor: | Yue Wu, Liu Liu, Rui Xu, Zhaosi Zhang, Han Liu, Xiaochuan Sun, Zongduo Guo, Wei-na Chai, Hongrong Zhang, Junchi He, Chongjie Cheng, Li Jiang, Zhijian Huang, Gang Huo, Jianjun Zhong |
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| Rok vydání: | 2018 |
| Předmět: |
Male
medicine.medical_specialty Traumatic brain injury medicine.disease_cause Gastroenterology Neuroprotection Lesion Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine 030225 pediatrics Internal medicine Brain Injuries Traumatic medicine oxidative stress Animals Humans Cerebral perfusion pressure Retrospective Studies business.industry traumatic brain injury Glasgow Outcome Scale General Medicine Middle Aged Prognosis medicine.disease Uric Acid Mice Inbred C57BL Disease Models Animal chemistry Cerebral blood flow inflammation Uric acid Female UA (uric acid) medicine.symptom business 030217 neurology & neurosurgery Oxidative stress Research Paper |
| Zdroj: | International Journal of Medical Sciences |
| ISSN: | 1449-1907 |
| Popis: | Background: As a major antioxidant in serum, uric acid (UA) was once considered only as the leading cause of gout; however, recent studies have validated its neuroprotective role in ischemic stroke. Because the potential protective effects of UA in traumatic brain injury (TBI) remain largely unknown, this study investigated the role of UA in TBI in both clinical patients and experimental animals. Methods: In TBI patients, serum UA concentrations were measured within 3 days after injury. Clinical outcomes at discharge were classified according to the Glasgow Outcome Scale: good outcome (4-5) and poor outcome (1-3). Risk factors for good outcome were identified via backward logistic regression analysis. For the animal study, a controlled cortical impact (CCI) injury model was established in mice. These mice were given UA at different doses intraperitoneally, and subsequent UA concentrations in mouse serum and brain tissue were determined. Neurological function, oxidative stress, inflammatory response, neuronal maintenance, cerebral blood flow, and lesion size were also assessed. Results: The serum UA level was significantly lower in TBI patients who had a good outcome (P0.05). Conclusions: UA acted to attenuate neuronal loss, cerebral perfusion impairment and neurological deficits in TBI mice through suppression of neuronal and vascular oxidative stress. Following TBI, active antioxidant defense in the brain may result in consumption of UA in the serum, and thus, a decreased serum UA level could be predictive of good clinical recovery. |
| Databáze: | OpenAIRE |
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