BACKGROUND: Two-thirds partial hepatectomy (PHx) is an established model for the study of liver regeneration after resection. This process is accompanied by oxidative stress. AIMS: In our study, we tested the effect of epigallocatechin gallate (EGCG), a green tea antioxidant, on the early phase of liver regeneration after PHx. METHODS: Male Wistar rats were divided into five groups: (I) laparotomy + water for intraperitoneal injections, (II) laparotomy + EGCG 50 mg/kg body weight, (III) PHx + water for injections, (IV) PHx + EGCG 20 mg/kg and (V) PHx + EGCG 50 mg/kg, for 3 consecutive days. The rats were killed 24 h after surgery. Biochemical analysis of rat sera was performed. Histological samples were stained with hematoxylin & eosin and bromodeoxyuridine (BrdU). In hepatectomized rats, we also measured plasma malondialdehyde, tissue malondialdehyde, glutathione and cytokines levels, the activity of caspases 3/7, expression of Nqo-1 and HO-1 genes at the mRNA level, and expression of p21, p-p27 and p-p53 genes at the protein level. RESULTS: We observed lower accumulation of BrdU in group V when compared to groups III and IV. The activity of caspases 3/7 and expression of p-p53 were lower in group V than in groups III and IV. Tissue levels of IL-6 were lower in group V when compared to group III. Significant differences were not noted in other parameters. CONCLUSIONS: Administration of EGCG did not stimulate early phase liver regeneration in rats after PHx. There was even lower DNA synthesis in the group treated with a high dose of EGCG.

• MeSH
• Antioxidants pharmacology   therapeutic use   MeSH
• Cytokines genetics   metabolism   MeSH
• Heme Oxygenase-1 genetics   metabolism   MeSH
• Hepatectomy methods   MeSH
• Caspases genetics   metabolism   MeSH
• Catechin analogs & derivatives   pharmacology   therapeutic use   MeSH
• Rats MeSH
• RNA, Messenger genetics   metabolism   MeSH
• NAD(P)H Dehydrogenase (Quinone) genetics   metabolism   MeSH
• Oxidative Stress physiology   MeSH
• Rats, Wistar MeSH
• Cell Cycle Proteins genetics   metabolism   MeSH
• Liver Regeneration drug effects   MeSH
• Gene Expression Regulation drug effects   physiology   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Antioxidants MeSH
• Cytokines MeSH
• epigallocatechin gallate MeSH Browser
• Heme Oxygenase-1 MeSH
• Caspases MeSH
• Catechin MeSH
• RNA, Messenger MeSH
• NAD(P)H Dehydrogenase (Quinone) MeSH
• NQO1 protein, rat MeSH Browser
• Cell Cycle Proteins MeSH

Oxidative stress and mitochondrial dysfunction play an important role in the pathogenesis of nonalcoholic fatty liver disease and toxic liver injury. The present study was designed to evaluate the effect of exogenous inducer of oxidative stress (tert-butyl hydroperoxide, tBHP) on nonfatty and steatotic hepatocytes isolated from the liver of rats fed by standard and high-fat diet, respectively. In control steatotic hepatocytes, we found higher generation of ROS, increased lipoperoxidation, an altered redox state of glutathione, and decreased ADP-stimulated respiration using NADH-linked substrates, as compared to intact lean hepatocytes. Fatty hepatocytes exposed to tBHP exert more severe damage, lower reduced glutathione to total glutathione ratio, and higher formation of ROS and production of malondialdehyde and are more susceptible to tBHP-induced decrease in mitochondrial membrane potential. Respiratory control ratio of complex I was significantly reduced by tBHP in both lean and steatotic hepatocytes, but reduction in NADH-dependent state 3 respiration was more severe in fatty cells. In summary, our results collectively indicate that steatotic rat hepatocytes occur under conditions of enhanced oxidative stress and are more sensitive to the exogenous source of oxidative injury. This confirms the hypothesis of steatosis being the first hit sensitizing hepatocytes to further damage.

• MeSH
• Diet, High-Fat MeSH
• Glutathione metabolism   MeSH
• Hepatocytes drug effects   metabolism   MeSH
• Rats MeSH
• Cells, Cultured MeSH
• L-Lactate Dehydrogenase metabolism   MeSH
• Malondialdehyde metabolism   MeSH
• Membrane Potential, Mitochondrial drug effects   MeSH
• Non-alcoholic Fatty Liver Disease metabolism   pathology   MeSH
• Oxidative Stress drug effects   MeSH
• Lipid Peroxidation drug effects   MeSH
• Rats, Wistar MeSH
• Reactive Oxygen Species metabolism   MeSH
• tert-Butylhydroperoxide toxicity   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Glutathione MeSH
• L-Lactate Dehydrogenase MeSH
• Malondialdehyde MeSH
• Reactive Oxygen Species MeSH
• tert-Butylhydroperoxide MeSH