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Short‐term administration of (‐)‐epigallocatechin gallate reduces hepatic steatosis and protects against warm hepatic ischemia/reperfusion injury in steatotic mice
Author(s) -
Fiorini Ryan N.,
Donovan Jennifer L.,
Rodwell David,
Evans Zachary,
Cheng Gang,
May Harold D.,
Milliken Charles E.,
Markowitz John S.,
Campbell Crystal,
Haines Julia K.,
Schmidt Michael G.,
Chavin Kenneth D.
Publication year - 2005
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1002/lt.20348
Subject(s) - steatosis , medicine , energy charge , glutathione , reperfusion injury , endocrinology , pharmacology , intraperitoneal injection , ischemia , liver injury , fatty liver , antioxidant , biochemistry , chemistry , receptor , disease , adenylate kinase , enzyme
Hepatic steatosis increases the extent of cellular injury incurred during ischemia/reperfusion (I/R) injury. (‐)‐Epigallocatechin gallate (EGCG), the major flavonoid component of green tea ( camellia sinensis ) is a potent antioxidant that inhibits fatty acid synthase (FAS) in vitro. We investigated the effects of EGCG on hepatic steatosis and markers of cellular damage at baseline and after I/R injury in ob / ob mice. Animals were pretreated with 85 mg/kg EGCG via intraperitoneal (ip) injection for 2 days or oral consumption in the drinking water for 5 days before 15 minutes of warm ischemia and 24 hours of reperfusion. After EGCG administration, total baseline hepatic fat content decreased from baseline. Palmitic acid and linoleic acid levels also were reduced substantially in all ECGC‐treated animals before I/R. Alanine aminotransferase (ALT) levels decreased in all EGCG‐treated animals compared with control animals after I/R. Histologic analysis demonstrated an average decrease of 65% necrosis after EGCG administration. EGCG administration also increased resting hepatic energy stores as determined by an increase in cellular adenosine triphosphate (ATP) with a concomitant decrease in uncoupling protein 2 (UCP2) before I/R. Finally, there was an increased level of glutathione (GSH) in the EGCG‐treated mice compared with the vehicle‐treated mice both at baseline and after I/R. In conclusion, taken together, this study demonstrates that treatment with ECGC by either oral or ip administration, significantly protects the liver after I/R, possibly by reducing hepatic fat content, increasing hepatic energy status, and functioning as an antioxidant. (Liver Transpl 2005;11:298–308.)