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中药复方FBD提取物可预防脑缺血再灌注诱导的脑损伤和炎症。

Herbal formula FBD extracts prevented brain injury and inflammation induced by cerebral ischemia-reperfusion.

作者信息

Lin Zhihong, Zhu Danni, Yan Yongqing, Yu Boyang

机构信息

Department of Chinese Medicinal Prescription, China Pharmaceutical University, Nanjing, PR China.

出版信息

J Ethnopharmacol. 2008 Jun 19;118(1):140-7. doi: 10.1016/j.jep.2008.03.023. Epub 2008 Apr 11.

Abstract

The aim of this work was to verify neuroprotective and anti-inflammatory properties of FBD, a herbal formula composed of Poria cocos, Atractylodes macrocephala and Angelica sinensis, in ICR mice subjected to repetitive 10 min of common carotid arteries occlusion followed 24 h reperfusion. Intragastrical pretreatment with supercritical carbon dioxide extract (FBD-CO(2), 37.5 mg/kg) twice daily for 3.5 d, significantly reduced Evans Blue influx, neuron specific enolase (NSE) efflux, brain infarction (all p<0.05), also inhibited polymorphonuclear leukocytes (PMNs) infiltration (p<0.001), suppressed secretion of tumor necrosis factor (TNF)-alpha in blood (p<0.05), interleukin (IL)-1beta and IL-8 in brain (both p<0.01), and down-regulated cerebral expression of phosphor-IkappaB-alpha and phosphor-nuclear factor kappa-B (NF-kappaB), whether coupled with aqueous extract (FBD-H(2)O, 150 mg/kg) or not. Moreover, FBD-CO(2) (0.1-10 microg/ml) inhibited 0.1 microM phorbol myristate acetate-evoked oxidative burst in rat PMNs, 20 ng/ml TNF-alpha-triggered PMNs adhesion to ECV304 endothelial cells, and PMNs neurotoxicity to PC12 neuron-like cells as well as NSE release (IC(50) 1.30, 0.98, 0.24 and 0.82 microg/ml, respectively). Our study demonstrated that FBD-CO(2) prevented brain ischemia/reperfusion injury, at least in part, by limiting PMNs infiltration and neurotoxicity mediated by TNF-alpha, IL-1beta and IL-8, via inhibition on NF-kappaB activation.

摘要

本研究旨在验证茯苓、白术和当归组成的中药复方茯苓白术当归汤(FBD)对ICR小鼠反复10分钟颈总动脉闭塞并再灌注24小时后的神经保护和抗炎特性。每天两次用超临界二氧化碳提取物(FBD-CO₂,37.5毫克/千克)进行胃内预处理,持续3.5天,可显著减少伊文思蓝渗出、神经元特异性烯醇化酶(NSE)流出、脑梗死(均p<0.05),还可抑制多形核白细胞(PMN)浸润(p<0.001),抑制血液中肿瘤坏死因子(TNF)-α分泌(p<0.05)、脑内白细胞介素(IL)-1β和IL-8分泌(均p<0.01),并下调脑内磷酸化IκB-α和磷酸化核因子κB(NF-κB)的表达,无论是否联合水提取物(FBD-H₂O,150毫克/千克)。此外,FBD-CO₂(0.1-10微克/毫升)可抑制0.1微摩尔佛波醇肉豆蔻酸酯乙酸酯诱发的大鼠PMN氧化爆发、20纳克/毫升TNF-α触发的PMN与ECV304内皮细胞的黏附,以及PMN对PC12神经元样细胞的神经毒性和NSE释放(IC₅₀分别为1.30、0.98、0.24和0.82微克/毫升)。我们的研究表明,FBD-CO₂至少部分通过抑制NF-κB激活,限制由TNF-α、IL-1β和IL-8介导的PMN浸润和神经毒性,从而预防脑缺血/再灌注损伤。

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