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Protective effect of glycyrrhizic acid on cerebral ischemia/reperfusion injury via inhibiting HMGB1-mediated TLR4/NF-κB pathway.
Biotechnology and Applied Biochemistry ( IF 2.8 ) Pub Date : 2019-10-10 , DOI: 10.1002/bab.1825
Sunhong Yan 1 , Chuanqin Fang 1 , Lei Cao 1 , Long Wang 1 , Jing Du 1 , Yue Sun 1 , Xuanxia Tong 1 , Ying Lu 2 , Xiaosan Wu 1
Affiliation  

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.

中文翻译:

甘草酸通过抑制HMGB1介导的TLR4 /NF-κB途径对脑缺血/再灌注损伤的保护作用。

脑缺血是由多种疾病引起的,例如中风,心肌梗塞或周围血管疾病。本文的目的是研究甘草酸(GA)对脑缺血/再灌注(I / R)损伤的影响。建立大脑中动脉闭塞以评估GA对脑缺血的影响。在这项研究中,我们的结果表明,GA可以显着减少脑水肿,减少神经功能缺损,并且在GA治疗组中发现较小的脑梗塞体积。在血清和脑组织中,GA还增加了超氧化物歧化酶的活性。此外,在血清和脑组织中,GA还可以显着抑制炎性细胞因子的分泌,包括白介素-1β(IL-1β),IL-6和肿瘤坏死因子-α。而且,GA抑制高迁移率族蛋白盒1(HMGB1)介导的TLR4 /NF-κB通路的表达。我们的数据确定GA可能对I / R诱发的脑缺血疾病具有保护作用。
更新日期:2020-01-09
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