格列本脲
医学
小胶质细胞
磺酰脲受体
海马体
脑水肿
药理学
内科学
肿瘤坏死因子α
麻醉
内分泌学
炎症
糖尿病
作者
Ryuta KAJIMOTO,Takahiro Igarashi,Nobuhiro MORO,Hideki OSHIMA,Takeshi Suma,Naoki Otani,Atsuo Yoshino
出处
期刊:Journal of Neurosurgical Sciences
[Edizioni Minerva Medica]
日期:2023-07-01
卷期号:67 (4)
被引量:1
标识
DOI:10.23736/s0390-5616.22.05271-7
摘要
BACKGROUND: Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is a new therapeutic target. Sulfonylurea receptor 1 (SUR1) is expressed in nerve cells, glial cells, and vascular endothelial cells in EBI. SUR1 promotes intracellular inflow of Na and Ca ions, resulting in cell swelling and depolarization, and finally cell death. Glibenclamide reduced cerebral edema and mortality in a basic study of cerebral ischemia. However, the effects of glibenclamide on EBI have not been fully elucidated. This study examined the inhibitory effect of glibenclamide on EBI.METHODS: Rats were divided into the sham group, SAH-control group, and SAH-glibenclamide group. The water content of the brain was measured using the dry-wet method. In addition, the brain was divided into the cortex, putamen, and hippocampus, and expression of inflammatory cytokines was evaluated by the polymerase chain reaction method. In addition, microglia in the brain were evaluated immunohistologically.RESULTS: Water content of the brain was significantly decreased in the SAH-glibenclamide group compared to the SAH-control group. Interleukin-1beta (IL-1β), tumor necrosis factor alpha (TNFα), and nuclear factor-kappa B significantly increased in the cerebral cortex after SAH. IL-1β and TNFα in the cortex were significantly decreased in the SAH-glibenclamide group compared to the SAH-control group. Immunohistochemical staining confirmed that SAH causes extensive microglial activation in the brain, which was suppressed by glibenclamide.CONCLUSIONS: The present study showed that glibenclamide suppressed cerebral edema and activation of microglia and hypersecretion of inflammatory cytokines. Glibenclamide is a potential therapeutic method which may significantly improve the functional prognosis.
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