S期激酶相关蛋白2在肝再生组织中的表达及其意义

目的：观察S期激酶相关蛋白2(Skp2)在大鼠肝部分切除后残肝中的表达,探讨其在肝再生过程中的意义。方法：大鼠行70%肝部分切除术,分别在术后12,24,48,72,168 h,用免疫组化方法检测肝再生组织中Skp2及PCNA蛋白表达。结果：肝部分切除术后12,24,48,72 h,大鼠残肝组织中的Skp2及PCNA均表达明显增高,与相应各时间点的假手术组比较差异均有统计学意义(均P<0.01),且两者均在肝切除后48 h表达量达到最高峰,呈明显正相关(r=0.9085,P<0.05)。结论：Skp2在肝部分切除术后肝再生中起重要作用。     

The effect of a tumour necrosis factor antibody on the regenerative response after partial hepatectomy in rats

Abstract In this study we investigated the effect of tumour necrosis factor (TNF) on the regenerative response after partial hepatectomy. Adult male rats were injected intravenously with an antibody to TNF immediately after partial hepatectomy. Animals were sacrificed at 0, 24, 48, 72 and 96 h postoperatively. Hepatic thymidine kinase (TK) activity, liver weight to body weight (LW/BW) ratio, and mitotic index (MI) were used as indices of hepatic regeneration. The rats treated with TNF-Ab had significantly lower levels of TK activity in the liver at 24 h postoperatively compared to the saline treated animals. Furthermore the peak hepatic TK activity was delayed to 48 h in the rats treated with TNF-Ab. The mitotic indices and LW/BW ratios in the TNF-Ab- and saline-treated animals were similar. These data suggest that TNF potentiates the regenerative response after partial hepatectomy.     

Anabolic steroid nandrolone augments hepatic regenerative response in rats

The success of recovery after liver resection depends on the regeneration and functions of the remnant liver. In this study we investigated whether liver regeneration was facilitated by nandrolone decaonate after two-thirds partial hepatectomy in rats. Study animals were pretreated with nandrolone (5 mg/kg), while control animals received a placebo. Animal were sacrificed at 12, 24, 48, and 72 hours. We compared the survival rates, liver function tests as well as the amount of apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine-biotin nick end labeling assay, and regeneration, which was expressed as ratio of proliferating cell nuclear antigen and restoration ratio. A significant increase in hepatocyte regeneration at 24 and 48 hours in partially hepatectomized rats treated with nandrolone decaonate was observed compared to controls. This observation was confirmed by the significant acceleration of the liver restoration rate, which was 1/5 faster than in partially hepatectomized controls. The results of this study indicate that liver regeneration in rats treated with nandrolone show a prompt, faster regeneration after partial hepatectomy.     

Single dose of anti-transforming growth factor-beta1 monoclonal antibody enhances liver regeneration after partial hepatectomy in biliary-obstructed rats

BACKGROUND: Transforming growth factor (TGF) beta is a potent inhibitor of hepatocyte DNA synthesis and liver regeneration. TGF-beta(1) expression progressively increases in obstructive jaundice. We investigated the effect of TGF-beta(1) blockage on liver regeneration in rats induced with obstructive jaundice. MATERIALS AND METHODS: Male Wistar-albino rats were divided into three groups: sham, control, and study groups. In the study and control groups, the common bile duct was ligated and divided, and 7 days later a partial hepatectomy was performed. In the study group, anti-TGF-beta(1) monoclonal antibody (10-microg single dose) was administered immediately after the 70% hepatectomy. In the control group, those rats in which obstructive jaundice was induced received normal saline after the 70% hepatectomy, and nonjaundiced rats received anti-TGF-beta(1) monoclonal antibody after the 70% hepatectomy. Rats were sacrificed after 48 or 72 h. Relative liver weight, AST, ALT, total and conjugated bilirubin, and TGF-beta(1) levels were measured. The mitotic index and proliferating cell nuclear antigen (PCNA) labeling index were evaluated as histopathologic parameters. RESULTS: At 72 h, the TGF-beta(1) level in the study group was similar to that in the sham group, whereas TGF-beta(1) in the study group was significantly lower than that of the jaundiced control group at 48 or 72 h (P < 0.001). The relative liver weight, mitotic index, and PCNA labeling index were significantly higher in the study group than in the jaundiced control group at 48 and 72 h (P < 0.001). The AST, ALT, and TGF-beta(1) levels were significantly higher in the jaundiced control group compared to the study group after 48 and 72 h, whereas these values were significantly lower in the nonjaundiced control group (P < 0.001). CONCLUSIONS: In obstructive jaundiced rats, TGF-beta(1) blockage with anti-TGF-beta(1) monoclonal antibody after liver resection improved liver regeneration both morphologically and functionally.     

The effect of denervation on liver regeneration in partially hepatectomized rats

BACKGROUND/AIM: In a partial liver transplantation, the dissected hepatic nerves are left unrepaired during active liver regeneration. In fact, the pathophysiological influence of such hepatic denervation on liver regeneration has not yet been fully clarified. The aim of the present study is to elucidate the effect of total hepatic denervation on liver regeneration. METHODS: Experiment 1: To confirm the effect of hepatic denervation, the hepatic contents of norepinephrine were measured in both denervated (n = 5) and sham (n = 5) rats. The changes in the hepatic microcirculation were also measured in both denervated (n = 5) and sham (n = 5) rats. Experiment 2: The rats (n = 80) were randomly assigned to two groups: DN group (n = 40); hepatic denervation followed by a partial hepatectomy (PH). Control group (n = 40); sham hepatic denervation followed by PH. In both groups, the animals were killed at 12, 24, 36, 48, 72, 120, and 168 h after PH, respectively. The liver to body weight ratio and the proliferating cell nuclear antigen (PCNA) labeling index were measured at each time point. RESULTS: Experiment 1: Nearly a total depletion of norepinephrine (<99%) was observed in the DN rats. In addition, the hepatic tissue blood flow significantly increased in the DN rats. Experiment 2: The liver to body weight ratio of the DN group was also significantly higher than that of the control group at 168 h (P < 0.05). The PCNA labeling index peaked between 24 and 36 h in the control group, while that in the DN group showed a delayed peak. At 72 and 120 h, the PCNA labeling index was significantly higher in the DN group than in the control group (P < 0.05). CONCLUSION: Total hepatic denervation was thus found to enhance liver regeneration after a partial hepatectomy. This phenomenon is partially triggered by the increased hepatic blood flow to the remnant liver.     

Lack of protection of ischaemic preconditioning in the rat model of major hepatectomy with ischaemia reperfusion injury

OBJECTIVE: To investigate the effects of ischaemic preconditioning (IP) on residual liver regeneration after major hepatectomy without portal blood bypass in rats, and to verify whether it can protect the residual liver from ischaemia reperfusion (IR) injury. METHODS: Ninety rats were randomized into three groups: Group PH, rats were subjected to 70% hepatectomy alone; Group IR, rats were subjected to 30 minutes of total hepatic ischaemia, and 70% hepatectomy was performed just before reperfusion; Group IP, rats were pretreated with IP (5/10 minutes). During the preoperative period and at 0.5, 6, 12, 24 and 48 hours after the operation, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were measured using an autoanalyser. Serum hyaluronic acid (HA) was measured by radioimmunoassay. Regenerated liver weight (RLW) of the rats was measured and the expressions of Ki-67 and cyclin D1 were determined by immunohistochemistry in remnant liver tissue. RESULTS: There were no significant differences in serum AST and ALT levels in all the groups before the operation. After partial hepatectomy, AST and ALT levels increased rapidly. From 0.5 to 24 hours after operation, serum AST and ALT levels were significantly higher in IP group rats than in PH and IR rats (p < 0.05). There were no significant differences in serum HA levels in all the groups before the operation. After partial hepatectomy, HA levels increased rapidly, reaching peak values at 12 hours. In the early stage (during 12 hours) after the operation, HA level was significantly higher in IP rats than in PH and IR rats (p < 0.05). The RLW of the rats rapidly increased after partial hepatectomy, and significantly decreased in IP rats compared with PH and IR rats (p < 0.05). Cyclin D1 and Ki-67 expression in all groups before the operation were low and were not significantly different. After partial hepatectomy, they rapidly increased. The expression of Ki-67 and cyclin D1 reached a peak at 24 hours after the operation in PH rats, and they were significantly higher compared with IR and IP rats (p < 0.05). In groups IR and IP, the expression of cyclin D1 and Ki-67 reached peak values at 48 hours. A significant decrease (p < 0.05) was observed after 24 and 48 hours of reperfusion in group IP compared with groups PH and IR. CONCLUSION: IP impairs residual liver regeneration after major hepatectomy without portal blood bypass in rats, and protection from IR injury disappears. IP-induced hyperperfusion may be the cause of reduced liver regeneration.     

In vivo 31P NMR spectroscopic changes during liver regeneration

Liver regeneration following partial hepatectomy involves rapid cell division 24 to 72 hr postresection. This cell division would necessarily involve changes in intracellular energy stores and cell membrane phospholipid precursors. In tumor models 31P nuclear magnetic resonance (NMR) has been shown to identify intracellular substrate changes associated with cell growth. The ability to monitor early changes in adenosine triphosphate (ATP), inorganic orthophosphate (Pi), phosphomonoesters (PME), or phosphodiesters (PDE) after liver resection could indicate the intracellular changes necessary for hepatocellular regeneration. In vivo 31P NMR scans of the liver were performed in both normal rats and in rats at 24, 48, 72, and 120 hr after 70% hepatectomy. At 48 hr, total ATP fell to 18.9% (P less than 0.05) and both Pi/beta-ATP and PME/beta-ATP were significantly elevated (P less than 0.01) from controls. These changes correlate with the known mitotic peak in the rat following hepatectomy. We conclude that in vivo 31P NMR is a potentially valuable tool for studying hepatic regeneration. The data also suggest that hepatocellular regeneration may be critically dependent on cellular ATP stores.     

Total Blood Exchange Suppresses the Early Stage of Liver Regeneration Following Partial Hepatectomy in Rats

Despite its obscure and short effect, plasma exchange (PE) remains a mainstay in the treatment of liver disease. However, the question still remains as to whether or not PE suppresses the regeneration of the liver because PE deprives patients of hepatotrophic factors. The effect of PE, which could be a total blood exchange (TBE) in a syngeneic setting, on liver regeneration following a 68% partial hepatectomy (PH) was investigated in rats. In Group 1, 20 ml of blood from normal rats was infused while native blood was removed at 6 and 12 h after PH. In Group 2, 20 ml of blood obtained from PH rats at the same time points was infused. The regeneration rate, labeling index of proliferating cell nuclear antigen (PCNA), and plasma hepatocyte growth factor (HGF) level were determined, and standard liver function tests performed at 24, 48, and 72 h. Although all liver function tests improved in Group 1 at 24 and 48 h, the regeneration rate was significantly impaired. Similarly, the PCNA labeling index was significantly lower in Group 1 than that in Group 2. The plasma HGF level was significantly reduced in Group 1 (6 h blood out versus blood in: 1.1 ± 0.5 vs. 0.1 ± 0.1 ng/ml, p < 0.05). TBE with normal blood following PH suppressed the early stage of liver regeneration, in part, because of the reduction of HGF even though the blood was purified.     

Mechanism of liver regeneration after liver resection and portal vein embolization (ligation) is different?

Whether or not liver regeneration after portal branch embolization (PE) (ligation, PVL) in the non-embolized (ligated) lobe is by the same mechanism as regeneration in the remnant lobe after liver resection has been reviewed. Portal vein branch embolization and heat shock protein are then discussed. Tumor growth accelerated in the remnant liver after hepatectomy. In contrast, PE or PVL resulted in marked contralateral hepatic hypertrophy and significant reduction of tumor growth in the non-embolized (non-ligated) lobes. Follistatin administration significantly increased liver regeneration after hepatectomy in rats. In contrast, regeneration of non-ligated lobes after PVL was not accelerated by exogenous follistatin. Tumor growth also was not accelerated. The liver regeneration rate peaked at 48–72 h in the nonligated lobe after PVL, a delay of 24 h compared with the remnant liver after hepatectomy. In the postoperative early stage, the expression of activin βA, βC, and βE mRNAs was stronger in PVL than in hepatectomy. At 72 h the expression of activin receptor type IIA mRNA reached a peak in hepatectomy, but was significantly lower in PVL. Thus, regulation of activin signaling through receptors is one of the factors determining liver regeneration after hepatectomy and PVL. These serial experimental results imply that the mechanism of liver regeneration after portal branch ligation (embolization) is different from that after hepatectomy. Heat shock protein was induced in the liver experimentally by intermittent ischemic preconditioning and could play some beneficial role in the recovery of liver function after hepatectomy, even in cirrhotic patients. When heat shock protein following right portal vein embolization in both the embolized and non-embolized hepatic lobes was investigated in clinical cases, a two to fourfold increase in HSP70 was induced in the non-embolized lobe compared with the embolized lobe. Oral administration of geranylgeranylacetone (a non-toxic HSP inducer) suppressed inflammatory responses and improved survival after 95% hepatectomy by induction of HSP70 in rats.     

Expression of HGF and TGF-β1 mRNA after partial hepatectomy in rats with liver cirrhosis

Hepatocyte growth factor (HGF) is a potent mitogen for the maturation of hepatocytes in vitro which plays a role in liver regeneration in vivo. In addition, transforming growth factor-₁ (TGF-₁) is also a potent regulator of liver regeneration. In attempting to clarify the mechanisms related to liver regeneration after partial hepatectomy, we investigated the expression of HGF and TGF-₁ in rats with liver cirrhosis (LC). A rat model of LC was prepared using carbon tetrachloride (CCl₄). The expression of HGF mRNA in both the LC and control groups showed a similar time-course with the highest expression seen at 18 h after a 70% hepatectomy. The expression of TGF-₁ mRNA peaked at 18 h after partial hepatectomy in the LC group and at 48 h in the control group. The 5-bromo-2'-deoxyuridine (BrdU) labeling index for the LC group at 24, 48, and 72 h after partial hepatectomy was 9.2%, 5.9%, and 1.8%, while for the control group it was 7.0%, 11.7%, and 6.8%, respectively. The BrdU labeling index in the LC group was thus suppressed earlier than that in the control group. We therefore postulate that regeneration of the remnant liver in the presence of LC accelerates immediately after partial hepatectomy, but the extent of regeneration is insufficient because of an early cessation due to an early expression of TGF-₁.     

Anti-transforming growth factor-β1 antibody transiently enhances DNA synthesis during liver regeneration after partial hepatectomy in rats

The regulation of liver regeneration after partial hepatectomy (PHx) is complex and involves many different cytokines. We investigated the role of one of these, transforming growth factor-β1 (TGF-β1), an inhibitor of liver regeneration, in a Wistar male rat model, in which anti-TGF-β1 antibody was injected immediately or 24 h after 70% PHx. Livers from treated animals contained an increased number of cells in S phase, according to 5-bromo-2′-deoxyuridine (BrdU) labeling 36 h after PHx. Antibody administration 24 h after PHx resulted in the highest peak of proliferation; moreover, peak MIB-5 labeling was also observed at that time. However, neither residual liver-weight-to-body-weight ratios nor regeneration rates differed significantly between any of the animals. Therefore, we also measured levels of serum TGF-β1 and hepatocyte growth factor (HGF; an activator). With antibody administration at 0 or 24 h, TGF-β1 levels were diminished at 24 or 36 h as compared with levels in control rats, but then rebounded, reaching a delayed peak at 48 or 72 h after PHx, respectively. Interestingly, there were also similar trends in HGF levels. These results indicate that TGF-β1 may inhibit the G1 checkpoint, and serum TGF-β1 concentration may influence HGF to regulate liver regeneration and to maintain homeostasis of proliferation after PHx. Received: November 15, 2000 / Accepted: February 15, 2001     

Experimental study of the effect of intraportal prostaglandin E1 on hepatic blood flow during reperfusion after ischaemia and hepatectomy.

BACKGROUND: Prostaglandin E1 (PGE1) has protective effects experimentally and clinically in individual models of hepatic ischaemia-reperfusion injury and of partial hepatectomy. The present study investigated the effects of intraportal administration of PGE1 on hepatic blood flow, systemic arterial pressure and long-term animal survival after 60 min of total liver ischaemia followed by 70 per cent partial hepatectomy in rats. METHODS: Total liver ischaemia was induced by occluding the hepatoduodenal ligament for 60 min. PGE1 0.5 microg per kg per min was infused intraportally for 15 min before inducing ischaemia and for 120 min after ischaemia in the treatment group. Normal saline was infused in the control group. During ischaemia 70 per cent partial hepatectomy was performed. Portal venous flow (PVF), peripheral tissue blood flow (PTBF) and hepatic artery flow were measured before and after ischaemia. Serum biochemical analysis was carried out at 1, 3 and 24 h, and 7 and 14 days; and liver histology at 1 and 24 h, and 7 days after reperfusion. Survival was followed for 1 year. RESULTS: Intraportal infusion of PGE1 significantly improved PVF and PTBF without affecting the systemic arterial pressure. Long-term survival was significantly higher in the PGE1 group. Serum aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase levels decreased significantly, and 2-h bile flow was significantly improved, in the PGE1 group. Histological examination revealed significant portal venous congestion, sinusoidal congestion, fatty degeneration and tissue necrosis 24 h and 7 days after reperfusion in the control group. CONCLUSION: PGE1 has a protective effect against liver damage when the liver is injured by warm ischaemia and reperfusion followed by partial resection.     

Quantitative Gene Expression Analysis by cDNA Microarray During Liver Regeneration After Partial Hepatectomy in Rats

Purpose It is speculated that genetic regulation plays an important role during liver regeneration. We conducted this study to analyze quantitative gene expression during liver regeneration after partial hepatectomy.Methods Sixty male Wistar rats were randomly assigned into ten groups of six. One group of rats was killed preoperatively and the other nine groups were killed 2, 4, 6, 12, 24, 48, and 72h, and 5 and 7 days after 70% partial hepatectomy, respectively. The remnant livers were isolated for mRNA extraction. A mass survey of gene expression by cDNA microarray carrying 6144 polymerase chain reaction-amplified cDNA fragments was prepared by an arraying machine. The microarray images were scanned, digitized, and analyzed using a flatbed scanner.Results The variations in gene expression were classified into 72 different patterns including a pattern with a single peak, 2, 4, 6, 12, and 72h, and 5 and 7 days after partial hepatectomy. The other patterns included double peaks, enhancing trend, diminished trend, protruding curve, excavated curve, and various mixed types. Each category of gene expression pattern contained 40–218 different proto-oncogenes.Conclusion The quantitative gene expression profiles have important implications, warranting further investigation of the genetic mechanisms involved in the process of liver regeneration.     

Effect of splenectomy on liver regeneration and polyamine metabolism after partial hepatectomy

The effect of splenectomy on hepatic ornithine decarboxylase (ODC) induction, DNA synthesis, and mitosis of hepatocytes was studied in rat liver after partial hepatectomy. ODC activity markedly increased in the early stages of liver regeneration, and the increase in the activity was significantly enhanced in splenectomized rats. Splenectomy specifically induced ODC since tyrosine aminotransferase and general protein synthesis were not affected. Splenectomy also enhanced increase in hepatic polyamines, DNA synthesis, and mitosis in regenerating liver. The results suggest that splenectomy affects liver regeneration after partial hepatectomy by enhancing induction of ODC activity, which is an important biochemical event in the early stage of liver regeneration.     

Activin and activin receptor expression changes in liver regeneration in rat

BACKGROUND: This study aimed to investigate regulatory mechanisms of hepatocyte proliferation by comparing liver regeneration of the remnant lobe after 70% partial hepatectomy (PH) and portal vein branch ligation (PBL) in rat. METHODS: Expressions of activins betaA, betaC, and betaE and their receptors were investigated after PH and PBL. The proliferating cell nuclear antigen (PCNA) labeling index was used to monitor hepatocyte proliferation. RESULTS: The PCNA labeling index in the regenerative lobe of PBL rats reached a peak at 48 h, a delay of 24 h compared with the remnant lobe in PH rats. In the postoperative early stage, the expression of activin betaA, betaC, and betaE mRNAs was stronger in PBL than PH. At 72 h the expression of activin receptor type IIA mRNA reached a peak in PH but was significantly lower in PBL. CONCLUSIONS: Hepatocyte proliferation, and the regulated expression of activins and their receptors, differs during liver regeneration after PH and PBL in the rat. Thus, regulation of activin signaling through receptors is one of the factors determining liver regeneration after PH and PBL.     

Experimental study on tumor growth in the regenerating liver

The purpose of this study was to investigate the effect of liver regeneration on the growth of liver tumor. VX2 carcinoma was transplanted in the liver of New Zealand white rabbits, and 40% partial hepatectomy was performed. The following results were obtained. 1. After 40% partial hepatectomy VX2 carcinoma was transplanted in the remaining liver. Two weeks later, the tumor volume was larger in partially hepatectomized than in shamoperated rabbits (p less than 0.01). 2. When 40% hepatectomy of rabbits which carrying VX2 carcinoma transplanted 2 weeks previously was performed, the mitotic index of the tumor at 24 to 36 hours was significantly higher in hepatectomized than in sham-operated rabbits (p less than 0.02). At 24, 36, 48 hours after partial hepatectomy, the mitotic index of the hepatocytes of the hepatectomized group was significantly higher than that of sham-operated group (24 hrs.: p less than 0.005, 36 hrs.: p less than 0.01, 48 hrs.: p less than 0.005). 3. At 36 hours after partial hepatectomy there was a significant increase of DNA synthesis in tumor cells as compared with that in sham-operated controls (p less than 0.05). These data indicate that liver regeneration enhances the tumor growth in regenerating liver.     

Effect of partial portal vein ligation on hepatic regeneration

To evaluate the effect of portal hypertension and diminished portal venous blood flow to the liver on hepatic regeneration, male rats were subjected to partial portal vein ligation and subsequently to a two-thirds partial hepatectomy. The levels of ornithine decarboxylase activity at 6 h after partial hepatectomy were greater (p less than 0.001) in the rats with prior partial portal vein ligation than in those without portal hypertension. The rats with prior partial portal vein ligation also had greater (p less than 0.005) levels of thymidine kinase activity at 48 h after partial hepatectomy than did those without portal hypertension. Hepatic sex hormone receptor activity was not affected by prior partial portal vein ligation either before or after partial hepatectomy. The reductions in both estrogen and androgen receptor activity observed in the hepatic cytosol after partial hepatectomy were similar to those observed in control animals. These data indicate that animals with portal hypertension having a diminished hepatic portal blood flow have a normal capacity to regenerate hepatic mass following a hepatic resection.     

Augmentative effect of cyclosporin A on rat liver regeneration: influence on hepatocyte growth factor and transforming growth factor-beta(1).

We investigated the effect of cyclosporin A (CsA) on rat liver regeneration following partial hepatectomy with reference to cytokine production. Rats were divided into two groups: those without CsA pretreatment (group 1) and those with CsA pretreatment (group 2). Animals were given olive oil vehicle or CsA (10 mg/kg) dissolved in olive oil daily by gavage from 4 to 1 days before hepatectomy. The ratio of regenerating liver weight to initial body weight in group 2 was significantly higher than that in group 1 at 72 h. Although a peak 5-bromo-2-deoxyuridine labeling index was found at 24 h after hepatectomy in both groups, the peak value in the CsA-treated animals was significantly higher than in controls. In both groups, hepatocyte growth factor concentrations in both plasma and liver tissue showed maximal values at 12 h. Liver tissue values in group 2, however, were significantly higher from 1 to 12 h compared to group 1. Transforming growth factor-beta(1) (TGF-beta(1)) concentrations showed minimal serial changes in group 1, while those in liver tissue of group 2 rats were significantly lower than in group 1. Plasma TGF-beta(1) concentrations did not differ. These results suggest that upregulation of hepatic regeneration with CsA pretreatment might be attributed in part to changes in production of these mitogenic and mitoinhibitory cytokines.     

Effect of hyperbaric oxygen on liver regeneration in a rat model

Hyperbaric oxygen therapy is a treatment that has been gradually implemented for the treatment of several pathologic conditions. The present study evaluated the effect of hyperbaric oxygen therapy for hepatic regeneration and its relationship to mitochondrial function. Male Wistar rats underwent partial hepatectomy (70%) and subsequently underwent two sessions of hyperbaric oxygen (90 minutes each, at a pressure of 2 ATA). The animals were sacrificed at 24 and 48 hours after surgery. Hepatic regeneration was evaluated by the dry weight of the remaining liver, the hepatic regeneration rate, the hepatic DNA content, and the hepatocyte proliferation rate using the "proliferating cell nuclear antigen" (PCNA) content. Function of the mitochondria was evaluated by its oxygen consumption during respiratory states 3 and 4, its respiratory control ratio (RCR), its membrane potential, as well as its osmotic swelling. We also measured serum levels of aminotransferases. The results revealed an increased dry weight of the remaining liver, regeneration rate, and DNA content at 24 and 48 hours after hepatectomy. The hepatocyte proliferation rate was significantly higher among animals treated with hyperbaric oxygen therapy at 48 hours after surgery. There was no significant difference in aminotransferase levels. Mitochondrial respiration revealed reduced oxygen consumption in state 3 after 48 hours. These results demonstrated that hyperbaric oxygen stimulates hepatic regeneration at 24 and 48 hours after 70% hepatectomy. The effect of hyperbaric oxygen on hepatic tissue occurs without tissue damage and protects mitochondria after 48 hours.