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PubMed1987

Role of the hepatic branch of the vagus nerve in liver regeneration in rats.

The role of the vagus nerve in liver regeneration after partial hepatectomy was examined by comparing the effects of hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) with those of subdiaphragmatic vagotomy in rats. Hepatic vagotomy delayed but did not suppress the increase in the rate of hepatic DNA synthesis and the activity of thymidine kinase after partial hepatectomy. On the other hand, subdiaphragmatic vagotomy delayed and suppressed these indices. The time courses of restoration of liver DNA content after partial hepatectomy were not affected by hepatic vagotomy. However, this index was both delayed and suppressed in subdiaphragmatic vagotomized rats. Hepatic vagotomy did not affect the daily food intake or the body weight increase after partial hepatectomy. However, subdiaphragmatic vagotomy caused considerably more loss of food intake and body weight. There were no differences in the plasma insulin levels after partial hepatectomy among three groups. We concluded that a vagal specific effect is evident in the delay but fails to suppress liver regeneration.

Animals↗
PubMed2003

The effects of Korean red ginseng (ginseng radix rubra) on liver regeneration after partial hepatectomy in dogs.

We investigated the effects of the oral administration of Korean red ginseng (KRG) on morphologic change and function of liver in dogs. Fifteen adult mongrel dogs (n=15) were divided into three groups: a control group (40% hepatectomy, untreated), a 250 group (40% hepatectomy, 250 mg/kg of KRG, PO), and a 500 group (40% hepatectomy, 500 mg/kg of KRG, PO). The liver regeneration, histologic findings, CBC (WBC, RBC, PCV, and PLT), and liver function tests (AST, ALT, GGT, ALP, LDH, and T-bil) were examined during experiment. The liver regeneration rates were higher in treated groups than in the control group. But, there were no significant differences. All hematological values were within normal ranges except leukocyte counts for 3 days postoperatively. The levels of AST and ALT in the treated groups were significantly decreased compared to that in the control group (p<0.05). The numbers of degenerative cells and area of connective tissue were significantly decreased in the liver of the dog with KRG administration (p<0.01). On the basis of these results, we could conclude that KRG accelerate the liver regeneration and ameliorate the liver injury after hepatectomy in dogs.

Animals↗
PubMed2006

c-Jun/AP-1 controls liver regeneration by repressing p53/p21 and p38 MAPK activity.

The AP-1 transcription factor c-Jun is a key regulator of hepatocyte proliferation. Mice lacking c-Jun in the liver (c-jun (Deltali*)) display impaired liver regeneration after partial hepatectomy (PH). This phenotype correlates with increased protein levels of the cdk-inhibitor p21 in the liver. We performed PH experiments in several double-knockout mouse models to genetically identify the signaling events regulated by c-Jun. Inactivation of p53 in c-jun (Deltali*) mice abrogated both hepatocyte cell cycle block and increased p21 protein expression. Consistently, liver regeneration was rescued in c-jun (Deltali*) p21 (-/-) double-mutant mice. This indicated that c-Jun controls hepatocyte proliferation by a p53/p21-dependent mechanism. Analyses of p21 mRNA and protein expression in livers of c-jun (Deltali*) mice after PH revealed that the accumulation of p21 protein is due to a post-transcriptional/post-translational mechanism. We have investigated several candidate pathways implicated in the regulation of p21 expression, and observed increased activity of the stress kinase p38 in regenerating livers of c-jun (Deltali*) mice. Importantly, conditional deletion of p38alpha in livers of c-jun (Deltali*) mice fully restored hepatocyte proliferation and attenuated increased p21 protein levels after PH. These data demonstrate that c-Jun/AP-1 regulates liver regeneration through a novel molecular pathway that involves p53, p21, and the stress kinase p38alpha.

Animals↗
PubMed2005

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.

Activin Receptors↗
PubMed2006

Effect of liver regeneration after partial hepatectomy and ischemia-reperfusion on expression of growth factor receptors.

AIM: To investigate the effects of experimental partial hepatectomy and normothermic ischemia-reperfusion damage on the time course of the expression of four different growth factor receptors in liver regeneration. This is relevant due to the potential therapeutic use of growth factors in stimulating liver regeneration. METHODS: For partial hepatectomy (PH) 80% of the liver mass was resected in Sprague Dawley rats. Ischemia and reperfusion (I/R) were induced by occlusion of the portal vein and the hepatic artery for 15 min. The epidermal growth factor receptor, hepatic growth factor receptor, fibroblast growth factor receptor and tumour necrosis factor receptor-1 were analysed by immunohistochemistry up to 72 h after injury. Quantitative RT-PCR was performed at the time point of minimal receptor expression (24 h). RESULTS: In immunohistochemistry, EGFR, HGFR, FGFR and TNFR1 showed biphasic kinetics after partial hepatectomy with a peak up to 12 h, a nadir after 24 h and another weak increase up to 72 h. During liver regeneration, after ischemia and reperfusion, the receptor expression was lower; the nadir at 24 h after reperfusion was the same. To evaluate whether this nadir was caused by a lack of mRNA transcription, or due to a posttranslational regulation, RT-PCR was performed at 24 h and compared to resting liver. In every probe there was specific mRNA for the receptors. EGFR, FGFR and TNFR1 mRNA expression was equal or lower than in resting liver, HGFR expression after I/R was stronger than in the control. CONCLUSION: At least partially due to a post-transcriptional process, there is a nadir in the expression of the analysed receptors 24 h after liver injury. Therefore, a therapeutic use of growth factors to stimulate liver regeneration 24 h after the damage might be not successful.

Animals↗
PubMed1992

The microsomal monooxygenase system of regenerating liver. An examination of the role of estradiol in the demasculinization of drug metabolism produced by 2/3 partial hepatectomy.

Declines in total cytochrome P450 content and in monooxygenase activities associated with some male specific isozymes of cytochrome P450 have been reported in the rat following 2/3 partial hepatectomy (2/3 PH). In the present study, we examined the effects of 2/3 PH on hepatic microsomal monooxygenase activities towards testosterone, the alkoxyresorufins, p-nitrophenol and carbon tetrachloride in male rats. Levels of P450 apoproteins were determined by Western blot analysis. The effects of hepatectomy and sham operations on plasma growth hormone (GH) pulse profiles and the effects of a single acute dose of estradiol (E2) were studied to determine the role of these factors in 2/3 PH mediated changes in oxidative metabolism. 2/3 PH produced substantial decreases in testosterone hydroxylation at positions 16 alpha, 2 alpha and 7 alpha, but only a small decrease in hydroxylation at position 6 beta. Reductions in CYP 2C11 (P450h) and CYP 2A1 (P450a) expression were observed with Western blot analysis down to 19 and 41% of control values, respectively, but insignificant effects were observed on expression of CYP 3A (P450p family) proteins recognized by a polyclonal antibody raised against rat CYP 3A2 (P450pcn2). In contrast, acute E2 treatment caused a 2-fold increase in expression of CYP 2A1 apoprotein and significantly decreased expression of CYP 2E1 (P450j) apoprotein and dependent monooxygenase activities, but had no significant effect on expression of CYP 2C11. Both sham operations and 2/3 PH caused a temporary decrease in plasma GH concentrations, but secretion returned towards normal 24-48 hr after both operations. These data suggest that some factor other than GH or E2 must be involved in the selective suppression of some P450 isozymes observed after 2/3 PH.

Animals↗
PubMed2006

Predominance of released mitochondrial enzymes by partial hepatectomy-induced rat regenerating liver is controlled by hemodynamic changes and not related to mitochondrial damage.

OBJECTIVE: Serum activities of assumed organ-specific enzymes are useful protein markers in the diagnosis of necrotic liver diseases. However, after partial hepatectomy (PH) in rats, remaining hepatocytes proliferate to restore the lost liver mass, even when there is a drastic but selective elevation of serum enzyme activities. The aim of the present study was to elucidate the underlying mechanisms involved in this PH-induced enhancement of enzyme release. MATERIAL AND METHODS: Routine spectrophotometric methods were used to measure nine "marker" enzyme activities in sera, in effluents from isolated perfused livers, as well as in the incubation media used for liver slices and isolated cells from either sham-operated or 70%-PH rats. RESULTS: PH induced a drastic increase in serum activities of liver enzymes, predominantly of mitochondrial localization. In the control and 70%-PH groups, liver enzymes were differentially released by varying in vitro flow rate/liver mass ratio, using livers perfused at variable flow rates. This event was reversible and not associated with liver structural or functional alterations, but was dependent on the flow-bearing physical forces and independent of production of extra-hepatic factors. Liver slices and isolated cells were used to identify additional flow-independent enzyme release. The 70%-PH-induced drastic release of specific enzymes (predominantly those from mitochondria) could be mimicked in control livers by changing the hepatic blood flow/mass ratio, and closely resembled urea production by these livers. CONCLUSIONS: PH-induced effects were not associated with liver necrosis or mitochondrial dysfunction and evidenced previously unrecognized mechanisms controlling the rate of enzyme release into the bloodstream, which might have clear clinical implications.

Alanine Transaminase↗