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桑椹提取物对脂多糖诱导的肝损伤和炎症的改善作用。

Improvement of lipopolysaccharide-induced hepatic injuries and inflammation with mulberry extracts.

机构信息

Institute of Biochemistry and Biotechnology, Chung Shan Medical University, and Department of Clinical laboratory, Tai-An Hospital, Taichung, Taiwan, ROC.

出版信息

J Sci Food Agric. 2013 Jun;93(8):1880-6. doi: 10.1002/jsfa.5984. Epub 2012 Dec 12.

DOI:10.1002/jsfa.5984
PMID:23238799
Abstract

BACKGROUND

Mulberry water extracts (MWEs), which contain polyphenols including anthocyanins, have been used in traditional Chinese edible food. The hepatoprotective effects and molecular mechanisms of MWEs on acute liver failure induced by lipopolysaccharides (LPS) were investigated in vivo.

RESULTS

Rats were administered different doses of MWEs (0.5 and 1 g kg(-1)) 1 h before injection of LPS (5 mg kg(-1)) and then sacrificed 10 h after treatment with LPS. Liver function, inflammatory factors, oxidative stress index and hepatic histopathological alteration were examined in the rats with and without MWE treatment. Pretreatment with MWEs prevented LPS-induced liver damage by preventing associated increases of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALKP), triglycerol (TG), cholesterol and low-density lipoprotein/high-density lipoprotein ratio. MWEs also suppressed oxidative stress to prevent the formation of hepatic malondialdehyde (MDA). Furthermore, the molecular mechanism involved in LPS-induced liver injury was associated with reducing the expression of COX-2, NF-κB and iNOS in liver tissues.

CONCLUSION

The results support the investigation of MWEs as a therapeutic candidate for liver injuries and indicate that MWEs exhibit hepatoprotective activities via NF-κB signaling.

摘要

背景

桑椹水提取物(MWEs)含有包括花青素在内的多酚,已被用于中国传统食用食品中。本研究旨在体内研究 MWEs 对脂多糖(LPS)诱导的急性肝衰竭的肝保护作用及其分子机制。

结果

大鼠在注射 LPS(5mg/kg)前 1 小时给予不同剂量的 MWE(0.5 和 1g/kg),然后在 LPS 处理后 10 小时处死。在有和没有 MWE 处理的大鼠中检查了肝功能、炎症因子、氧化应激指标和肝组织病理学改变。MWE 预处理通过防止丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALKP)、甘油三酯(TG)、胆固醇和低密度脂蛋白/高密度脂蛋白比值的升高,预防 LPS 诱导的肝损伤。MWEs 还抑制氧化应激,防止肝组织丙二醛(MDA)的形成。此外,LPS 诱导的肝损伤的分子机制与降低肝组织中环氧化酶-2(COX-2)、核因子-κB(NF-κB)和诱导型一氧化氮合酶(iNOS)的表达有关。

结论

这些结果支持将 MWEs 作为治疗肝损伤的候选药物进行研究,并表明 MWEs 通过 NF-κB 信号通路发挥肝保护作用。

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