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叶下珠对酒精和多不饱和脂肪酸诱导的毒性纤维化标志物的保护作用。

Protective effects of Phyllanthus amarus on fibrotic markers during alcohol and polyunsaturated fatty acid-induced toxicity.

机构信息

Department of Biochemistry and Molecular Biology, Pondicherry University, Kalapet, Tamilnadu 605 014, India.

出版信息

Toxicol Mech Methods. 2011 Jan;21(1):48-52. doi: 10.3109/15376516.2010.529189. Epub 2010 Nov 3.

DOI:10.3109/15376516.2010.529189
PMID:21047178
Abstract

Alcoholic liver disease (ALD) remains a major problem, with significant morbidity and mortality worldwide. One of the serious consequences of ALD is hepatic fibrosis. This happens when the matrix synthesis rate exceeds that of matrix degradation. Matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) play a key role in matrix remodeling. Disruption of MMP/TIMP balance can lead to excessive accumulation of extracellular matrix components resulting in severe liver injury. The focus of the present study is to analyze the effect of Phyllanthus amarus on MMP and TIMPs activity in alcohol and thermally oxidized polyunsaturated fatty acid (PUFA)-induced hepatic fibrosis. Male albino Wistar rats were used for the study. The matrix metalloproteinase expression was found to be significantly decreased and the levels of TIMPs and the collagen were significantly increased in alcohol + thermally oxidized PUFA-treated rats. Administration of Phyllanthus amarus extract significantly decreased the levels of collagen and TIMPs; and positively modulated the expression of MMPs. From this study, we conclude that Phyllanthus amarus effectively modifies alcohol + thermally oxidized PUFA-induced fibrosis.

摘要

酒精性肝病(ALD)仍然是一个主要问题,在全球范围内发病率和死亡率都很高。ALD 的严重后果之一是肝纤维化。当基质合成率超过基质降解率时,就会发生这种情况。基质金属蛋白酶(MMPs)和基质金属蛋白酶抑制剂(TIMPs)在基质重塑中发挥关键作用。MMP/TIMP 平衡的破坏可导致细胞外基质成分的过度积累,从而导致严重的肝损伤。本研究的重点是分析叶下珠对酒精和热氧化多不饱和脂肪酸(PUFA)诱导的肝纤维化中 MMP 和 TIMPs 活性的影响。本研究使用雄性白化 Wistar 大鼠进行。结果发现,酒精+热氧化 PUFA 处理的大鼠中基质金属蛋白酶的表达明显降低,TIMP 水平和胶原明显升高。叶下珠提取物的给药显著降低了胶原和 TIMPs 的水平;并积极调节 MMPs 的表达。从这项研究中,我们得出结论,叶下珠能有效调节酒精+热氧化 PUFA 诱导的纤维化。

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