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甘草酸通过抑制 HMGB1 介导体 TLR4/NF-κB 通路对脑缺血再灌注损伤的保护作用。

Protective effect of glycyrrhizic acid on cerebral ischemia/reperfusion injury via inhibiting HMGB1-mediated TLR4/NF-κB pathway.

机构信息

Department of Neurology, The Second Hospital of Anhui Medical University, Hefei, People's Republic of China.

Department of Laboratory Medicine, The First Hospital of Nanjing Medical University, Nanjing, People's Republic of China.

出版信息

Biotechnol Appl Biochem. 2019 Nov;66(6):1024-1030. doi: 10.1002/bab.1825. Epub 2019 Oct 10.

DOI:10.1002/bab.1825
PMID:31545873
Abstract

Cerebral ischemia is caused by various disorders, such as stroke, myocardial infarction, or peripheral vascular disease. The purpose of this paper was to investigate the effects of glycyrrhizic acid (GA) on cerebral ischemia/reperfusion (I/R) injury. Middle cerebral artery occlusion was established to evaluate the effects of GA on cerebral ischemia. In this study, our results showed that GA could dramatically decrease cerebral edema, reduce the neurological deficits, and smaller brain infarct volume was found in the GA treatment group. In serum and brain tissue, GA also increased superoxide dismutase activity. In addition, in serum and brain tissue, GA also dramatically inhibited the secretion of inflammatory cytokines, including interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α. Moreover, GA inhibited the expressions of high-mobility group protein box-1 (HMGB1)-mediated TLR4/NF-κB pathway. Our data determined that GA may provide protective effect on the I/R-induced cerebral ischemia disease.

摘要

脑缺血是由各种疾病引起的,如中风、心肌梗死或外周血管疾病。本文旨在研究甘草酸(GA)对脑缺血/再灌注(I/R)损伤的影响。通过大脑中动脉闭塞来评估 GA 对脑缺血的影响。在这项研究中,我们的结果表明,GA 能显著减轻脑水肿,降低神经功能缺损,GA 治疗组的脑梗死体积更小。在血清和脑组织中,GA 还能显著增加超氧化物歧化酶的活性。此外,GA 还能显著抑制包括白细胞介素-1β(IL-1β)、IL-6 和肿瘤坏死因子-α在内的炎症细胞因子的分泌。此外,GA 抑制了高迁移率族蛋白 box-1(HMGB1)介导的 TLR4/NF-κB 通路的表达。我们的数据表明,GA 可能对 I/R 诱导的脑缺血疾病提供保护作用。

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