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Effects of compound Ginkgo bilobaon intestinal permeability in rats with alcohol-induced liver injury
This study aimed to investigate the effects of Compound Ginkgo biloba(CGB) on alterations in intestinal permeability and inflammation caused by endotoxin in chronic alcohol-induced liver injury. CGB was prepared by Ginkgo bilobaextract and Rosa roxburghiiin a 1 : 1 proportion. Rats were divided into...
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Published in: | Food & function 2015-02, Vol.6 (2), p.470-478 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | This study aimed to investigate the effects of Compound Ginkgo biloba(CGB) on alterations in intestinal permeability and inflammation caused by endotoxin in chronic alcohol-induced liver injury. CGB was prepared by Ginkgo bilobaextract and Rosa roxburghiiin a 1 : 1 proportion. Rats were divided into four groups: control, ethanol, high-dosage CGB (0.6 g kg super(-1) d super(-1)) and low-dosage CGB (0.2 g kg super(-1) d super(-1)) group. Rats in the control group ingested a Lieber-DeCarli control liquid diet, while rats in the ethanol and CGB-treated groups ingested a Lieber-DeCarli alcohol liquid diet for eight weeks. CGB was orally administered from the beginning of the third week until the end of the experiment. CGB was observed to significantly reduce the activities of serum ALT, AST, diamine oxidase (DAO) as well as levels of serum TG, d-lactic acid and plasma endotoxin in rats fed with Lieber-DeCarli ethanol liquid. Further, the hepatic steatosis was improved and the damage to intestinal tight junctions was also relieved effectively after CGB administration. Moreover, CGB significantly downregulated the expressions of TNF- alpha , lipopolysaccharide binding protein (LBP), CD14 and TLR4 in the liver and upregulated the expressions of tight junction proteins including ZO-1, occludin and claudin-1. In summary, this study demonstrated that CGB alleviated alcohol-induced liver injury and hepatic lipopolysaccharide signaling as well as gut barrier dysfunction through restoring tight junctions. |
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ISSN: | 2042-6496 2042-650X |
DOI: | 10.1039/c4fo00739e |