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BRP,一种从肉苁蓉中分离得到的多糖组分,可保护小鼠免受半乳糖胺和脂多糖诱导的肝衰竭。

BRP, a polysaccharide fraction isolated from Boschniakia rossica, protects against galactosamine and lipopolysaccharide induced hepatic failure in mice.

机构信息

Department of Biochemistry and Molecular Biology, Medical College of Yanbian University, Yanji, Jilin Province 133000, China ; Department of Physiology and Pathophysiology, Medical College of Yanbian University, Yanji, Jilin Province 133000, China.

Department of Biochemistry and Molecular Biology, Medical College of Yanbian University, Yanji, Jilin Province 133000, China.

出版信息

J Clin Biochem Nutr. 2014 May;54(3):181-9. doi: 10.3164/jcbn.13-105. Epub 2014 Apr 4.

Abstract

The aim of this study was to investigate the hepatoprotective effect of BRP, a polysaccharide fraction isolated from Boschniakia rossica, against galactosamine and lipopolysaccharide induced fulminant hepatic failure. Mice were injected with a single dose of galactosamine/lipopolysaccharide with or without pretreatment of BRP. Results showed marked reduction of hepatic necrosis, serum marker enzymes and levels of tumor necrosis factor-α and interleukin-6 in BRP pretreated mice when compared with galactosamine/lipopolysaccharide-challenged mice. Mice pretreated with BRP decreased the activation of caspases-3 and caspase-8, and showed a reduced level of DNA fragmentation of liver cells. BRP also reduced hepatic lipid peroxidation, increased potential of hepatic antioxidative defense system, and reduced hepatic nitric oxide level which was elevated by galactosamine/lipopolysaccharide injection. Immunoblot analysis showed down-regulation of inducible nitric oxide synthase and cyclooxygenase-2 proteins of liver tissues in BRP pretreated group when compared with galactosamine/lipopolysaccharide-challenged group. Furthermore, treatment with galactosamine/lipopolysaccharide markedly increased toll-like receptor 4, nuclear level of nuclear factor-κB, and phosphorylation of both extracellular signal-regulated kinase and c-Jun N-terminal kinase in liver tissues. However, these increases were attenuated by pretreatment with BRP. The results suggest that BRP alleviates galactosamine/lipopolysaccharide-induced liver injury by enhancing antioxidative defense system, suppressing inflammatory responses and reducing apoptotic signaling.

摘要

本研究旨在探讨从肉苁蓉中分离得到的多糖 BRP 对半乳糖胺和脂多糖诱导的暴发性肝衰竭的肝保护作用。小鼠单次注射半乳糖胺/脂多糖,并用 BRP 预处理或不预处理。结果表明,与半乳糖胺/脂多糖攻击组相比,BRP 预处理组小鼠肝坏死、血清标志物酶及肿瘤坏死因子-α和白细胞介素-6水平明显降低。BRP 预处理可降低 caspase-3 和 caspase-8 的激活,减少肝细胞 DNA 片段化。BRP 还可降低肝脂质过氧化,增加肝抗氧化防御系统的潜力,并降低半乳糖胺/脂多糖注射引起的肝一氧化氮水平。免疫印迹分析显示,与半乳糖胺/脂多糖攻击组相比,BRP 预处理组肝组织诱导型一氧化氮合酶和环氧化酶-2 蛋白表达下调。此外,用半乳糖胺/脂多糖处理可显著增加肝组织 Toll 样受体 4、核因子-κB 的核水平以及细胞外信号调节激酶和 c-Jun N-末端激酶的磷酸化。然而,这些增加被 BRP 预处理所减弱。结果表明,BRP 通过增强抗氧化防御系统、抑制炎症反应和减少凋亡信号来缓解半乳糖胺/脂多糖诱导的肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd0e/4042147/804cd38e996f/jcbn13-105f01.jpg

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