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咖啡可预防大鼠 CCl(4)-诱导的肝硬化。

Coffee prevents CCl(4)-induced liver cirrhosis in the rat.

机构信息

Departamento de Farmacología, Cinvestav-IPN, Apdo. Postal 14-740, 07000, México, DF, México.

出版信息

Hepatol Int. 2011 Sep;5(3):857-63. doi: 10.1007/s12072-010-9247-6. Epub 2011 Jan 25.

DOI:10.1007/s12072-010-9247-6
PMID:21484136
Abstract

PURPOSE

Previous clinical observations suggested that coffee may have beneficial effects on the liver. In fact, an inverse relationship between coffee consumption and liver cirrhosis has been reported in humans. However, the causative role of coffee has not been established; therefore, the aim of this work was to study the effect of coffee in an experimental model of liver damage.

METHODS

In this work, cirrhosis was induced by chronic CCl(4) administration and soluble or grain coffee (SC, GC, respectively) were co-administered for 8 weeks.

RESULTS

CCl(4) administration elevated serum alkaline phosphatase and alanine aminotranspherase, liver lipid peroxidation, collagen content (fourfold) and TGF-β mRNA, and protein levels; depleted liver glycogen and reduced glutathione (GSH) content. Coffee prevented most of the changes produced by CCl(4). Histopathological analysis was in agreement with biochemical and molecular data. The best effect was produced by GC. It is worth noting that GC preserved the normal collagen content as well as the normal TGF-β mRNA and protein levels.

CONCLUSIONS

Our results suggest (1) that coffee plays a causative role in preventing cirrhosis (at least experimental cirrhosis); (2) that action mechanisms are probably associated with down regulation of the profibrogenic cytokine TGF-β and to its antioxidant properties and, (3) that GC is more potent than SC. These findings suggest a beneficial effect of coffee on the liver. However, more clinical and basic studies must be performed before reaching a final recommendation.

摘要

目的

先前的临床观察表明,咖啡可能对肝脏有益。事实上,人类中已有研究报道咖啡摄入与肝硬化之间呈负相关关系。但是,咖啡的致病作用尚未得到证实;因此,本研究旨在探讨咖啡对实验性肝损伤模型的影响。

方法

本研究采用慢性 CCl4 给药诱导肝硬化,并同时给予可溶性或粒状咖啡(SC、GC)共给药 8 周。

结果

CCl4 给药导致血清碱性磷酸酶和丙氨酸氨基转移酶升高,肝脂质过氧化、胶原含量(增加四倍)和 TGF-β mRNA 及蛋白水平升高,肝糖原和还原型谷胱甘肽(GSH)含量降低。咖啡预防了 CCl4 引起的大多数变化。组织病理学分析与生化和分子数据一致。GC 产生的效果最佳。值得注意的是,GC 维持了正常的胶原含量以及正常的 TGF-β mRNA 和蛋白水平。

结论

我们的结果表明:(1)咖啡在预防肝硬化(至少是实验性肝硬化)方面起致病作用;(2)其作用机制可能与下调促纤维化细胞因子 TGF-β及其抗氧化特性有关,(3)GC 比 SC 更有效。这些发现提示咖啡对肝脏有益。但是,在提出最终建议之前,必须进行更多的临床和基础研究。

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Pharmacological application of caffeine inhibits TGF-beta-stimulated connective tissue growth factor expression in hepatocytes via PPARgamma and SMAD2/3-dependent pathways.咖啡因的药理学应用通过PPARγ和SMAD2/3依赖性途径抑制转化生长因子β刺激的肝细胞中结缔组织生长因子的表达。
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The antifibrotic and fibrolytic properties of date fruit extract via modulation of genotoxicity, tissue-inhibitor of metalloproteinases and nuclear factor- kappa B pathway in a rat model of hepatotoxicity.枣果提取物通过调节遗传毒性、金属蛋白酶组织抑制剂和核因子-κB途径对肝毒性大鼠模型的抗纤维化和促纤溶特性。
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