Inhibition of nitric oxide synthase aggravates brain injury in diabetic rats with traumatic brain injury |
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Authors: | Wan-Chao Yang Hong-Ling Cao Yue-Zhen Wang Ting-Ting Li Hong-Yu Hu Qiang Wan Wen-Zhi Li |
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Affiliation: | 1.Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China;2.Department of Anesthesiology, Jilin Province Tumor Hospital, Changchun, Jilin Province, China |
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Abstract: | Studies have shown that hyperglycemia aggravates brain damage by affecting vascular endothelial function. However, the precise mechanism remains unclear. Male Sprague-Dawley rat models of diabetes were established by a high-fat diet combined with an intraperitoneal injection of streptozotocin. Rat models of traumatic brain injury were established using the fluid percussion method. Compared with traumatic brain injury rats without diabetic, diabetic rats with traumatic brain injury exhibited more severe brain injury, manifested as increased brain water content and blood-brain barrier permeability, the upregulation of heme oxygenase-1, myeloperoxidase, and Bax, the downregulation of occludin, zona-occludens 1, and Bcl-2 in the penumbra, and reduced modified neurological severity scores. The intraperitoneal injection of a nitric oxide synthase inhibitor N(5)-(1-iminoethyl)-L-ornithine(10 mg/kg) 15 minutes before brain injury aggravated the injury. These findings suggested that nitric oxide synthase plays an important role in the maintenance of cerebral microcirculation, including anti-inflammatory, anti-oxidative stress, and anti-apoptotic activities in diabetic rats with traumatic brain injury. The experimental protocols were approved by the Institutional Animal Care Committee of Harbin Medical University, China(approval No. ky2017-126) on March 6, 2017. |
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Keywords: | apoptosis blood-brain barrier brain edema diabetes mellitus inflammation injury neurological function nitric oxide synthase traumatic brain injury |
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