Glycine protects isolated hepatocytes against anoxia and cystamine, but does not prevent rat liver injury associated with ischemia/reperfusion ‘in vivo’

1995 ◽  
Vol 31 ◽  
pp. 93-93
Author(s):  
M VAIRETTI ◽  
R IMBERTI ◽  
M GUALEA ◽  
G POMA ◽  
P RICHELMI ◽  
...  
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Isolated Hepatocytes

Mechanisms of conversion of xanthine dehydrogenase to xanthine oxidase in ischemic rat liver and kidney

1988 ◽  
Vol 254 (5) ◽  
pp. G753-G760 ◽  
Author(s):  
T. G. McKelvey ◽  
M. E. Hollwarth ◽  
D. N. Granger ◽  
T. D. Engerson ◽  
U. Landler ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Xanthine Dehydrogenase ◽  
Serum Glutamic Oxaloacetic Transaminase ◽  
Liver Model ◽  
Damage Process ◽  
Liver And Kidney ◽  
Sulfhydryl Modification

Previous studies have proposed and supported a role for the proteolytic, irreversible conversion of xanthine dehydrogenase to xanthine oxidase (XO) in postischemic injury in a wide variety of organs. A second mechanism of conversion, due to sulfhydryl modification and reversible with dithiothreitol (DTT), is potentially important but has not been well investigated. In this study rat liver and kidney were found to produce significant amounts of DTT-reversible XO during normothermic global ischemia. Formation of reversible XO precedes that of irreversible XO by approximately 0.5 h with a strong correlation (r = 0.92) existing between the rate of irreversible XO formation and the concentration of reversible XO. The formation of reversible XO is preceded by a depletion of glutathione with concentrations of glutathione during ischemia correlating (r = 0.85) with the observed concentration of reversible XO. While a large increase in the extent of liver damage occurs concurrently with conversion in an in vivo liver model of liver ischemia, an ischemia-reperfusion regimen (1 h of ischemia plus 0.5 h of reperfusion) that resulted in no conversion caused significant elevations in serum glutamic pyruvic transaminase and serum glutamic-oxaloacetic transaminase. Rats depleted of XO by tungsten dieting release 65% less enzyme after the same insult, suggesting that endogenous XO may also participate in the damage process independent of any conversion.

Role of neutrophils in ischemia/reperfusion liver injury. A study in the isolated perfused rat liver

1991 ◽  
Vol 13 ◽  
pp. S109
Author(s):  
O. Chazouillères ◽  
C. Legendre ◽  
M. Vaubourdolle ◽  
M.T. Bonnefis ◽  
C. Rey ◽  
...  
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver

Neutrophils contribute to ischemia/reperfusion injury in rat liver in vivo

1990 ◽  
Vol 4 (15) ◽  
pp. 3355-3359 ◽  
Author(s):  
Hartmut Jaeschke ◽  
Anwar Farhood ◽  
C. Wayne Smith
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Polyribosomes in isolated liver cells. Preparative procedures, effects of incubation and correlation with protein synthesis

1980 ◽  
Vol 186 (1) ◽  
pp. 35-45 ◽  
Author(s):  
A J Dickson ◽  
C I Pogson
Keyword(s):  
Protein Synthesis ◽  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Liver Cells ◽  
Liver Protein ◽  
Isolated Cells ◽  
Isolated Liver Cells ◽  
Rat Liver Cells ◽  
Isolated Liver

Methods have been derived which permit the isolation of undergraded polyribosomes from isolated rat liver cells. Under the conditions used the polyribosome profile of hepatocytes immediately after isolation was essentially identical with that from intact liver. However, during incubation of cells in complex physiological media there was a progressive dissociation of polyribosomes. The addition of a variety of factors that produce reaggregation of polyribosomes in rat liver in vivo did not prevent dissociation during cell incubations. Although large polyribosomes were lost most rapidly, the albumin-synthesizing capacity of isolated cells was not selectively lost when compared with total protein synthesis. The significance of these results for the use of isolated hepatocytes in the study of liver protein synthesis is discussed.

In vivo generation of free radical in ischemia-reperfusion in the rat liver

1990 ◽  
Vol 9 ◽  
pp. 96
Author(s):  
Anthony Koo ◽  
Gongming Tao ◽  
Neil Kaplowitz
Keyword(s):  
Free Radical ◽  
Rat Liver ◽  
Ischemia Reperfusion

In Vivo 19F Mr Spectroscopic Study of Metabolism of 5-Fluorotryptophan in Rat Liver

1992 ◽  
Vol 33 (3) ◽  
pp. 258-261 ◽  
Author(s):  
M. Harada ◽  
H. Nishitani ◽  
K. Koga ◽  
I. Miura ◽  
R. Kido
Keyword(s):  
Chemical Shift ◽  
Liver Injury ◽  
Spectroscopic Study ◽  
Rat Liver ◽  
Mr Spectroscopy ◽  
Renal Excretion ◽  
Normal Liver ◽  
Injury Group ◽  
Injured Liver

The metabolism of 5-fluorotryptophan in rat liver was examined by in vivo 19F MR spectroscopy. After i.v. injection of 200 mg/kg b.w. of 5-fluorotryptophan the substance was noted immediately as a strong peak, which decreased gradually. Another peak appeared about 40 min after the injection. The chemical shift value of this peak was 1.6 ppm from that of 5-fluorotryptophan. Kynurenine is known to be a major metabolite of tryptophan in the liver. We synthesized 5-fluorokynurenine from 5-fluorotryptophan by ozonolysis. The chemical shift value of 5-fluorokynurenine was confirmed to be coincident with that of the metabolite peak. This strongly suggests that the metabolite peak of 5-fluorotryptophan observed in this study was the 5-fluorokyrurenine signal. We also applied this method for the CCl4-injured liver. In the liver injury group, the metabolite peak appeared slowly and the intensity was low compared to that of the normal group, though the peak of 5-fluorotryptophan decreased similarly as in the normal liver. These results suggest that the decrease of 5-fluorotryptophan is due mainly to the renal excretion, as the injured liver could not metabolize 5-fluorotryptophan.

scholarly journals Acidic Microenvironment Aggravates the Severity of Hepatic Ischemia/Reperfusion Injury by Modulating M1-Polarization Through Regulating PPAR-γ Signal

2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Ding ◽  
Yunfei Duan ◽  
Zhen Qu ◽  
Jiawei Feng ◽  
Rongsheng Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Acidic Microenvironment ◽  
Ppar Γ ◽  
M1 Polarization ◽  
Hepatic Ischemia Reperfusion

Hepatic injury induced by ischemia and reperfusion (HIRI) is a major clinical problem after liver resection or transplantation. The polarization of macrophages plays an important role in regulating the severity of hepatic ischemia/reperfusion injury. Recent evidence had indicated that the ischemia induces an acidic microenvironment by causing increased anaerobic glycolysis and accumulation of lactic acid. We hypothesize that the acidic microenvironment might cause the imbalance of intrahepatic immunity which aggravated HIRI. The hepatic ischemia/reperfusion injury model was established to investigate the effect of the acidic microenvironment to liver injury. Liposomes were used to deplete macrophages in vivo. Macrophages were cultured under low pH conditions to analyze the polarization of macrophages in vitro. Activation of the PPAR-γ signal was determined by Western blot. PPAR-γ agonist GW1929 was administrated to functionally test the role of PPAR-γ in regulating macrophage-mediated effects in the acidic microenvironment during HIRI. We demonstrate that acidic microenvironment aggravated HIRI while NaHCO3 reduced liver injury through neutralizing the acid, besides, liposome abolished the protective ability of NaHCO3 through depleting the macrophages. In vivo and vitro experiment showed that acidic microenvironment markedly promoted M1 polarization but inhibited M2 polarization of macrophage. Furthermore, the mechanistic study proved that the PPAR-γ signal was suppressed during the polarization of macrophages under pH = 6.5 culture media. The addition of PPAR-γ agonist GW1929 inhibited M1 polarization under acidic environment and reduced HIRI. Our results indicate that acidic microenvironment is a key regulator in HIRI which promoted M1 polarization of macrophages through regulating PPAR-γ. Conversely, PPAR-γ activation reduced liver injury, which provides a novel therapeutic concept to prevent HIRI.

scholarly journals Graptopetalum paraguayense Inhibits Liver Fibrosis by Blocking TGF-β Signaling In Vivo and In Vitro

2019 ◽  
Vol 20 (10) ◽  
pp. 2592 ◽  
Author(s):  
Wei-Hsiang Hsu ◽  
Se-Chun Liao ◽  
Yau-Jan Chyan ◽  
Kai-Wen Huang ◽  
Shih-Lan Hsu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Rat Liver ◽  
Injury Model ◽  
Ethanol Extracts ◽  
And Migration ◽  
Tgf Β1

Background and Aims: Liver fibrosis is the excessive accumulation of extracellular matrix proteins, including collagen, which occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension. Activated hepatic perivascular stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines, such as TGF-β1. The inhibition of TGF-β1 function or synthesis is a major target for the development of antifibrotic therapies. Our previous study showed that the water and ethanol extracts of Graptopetalum paraguayense (GP), a Chinese herbal medicine, can prevent dimethylnitrosamine (DMN)-induced hepatic inflammation and fibrosis in rats. Methods: We used rat hepatic stellate HSC-T6 cells and a diethylnitrosamine (DEN)-induced rat liver injury model to test the potential mechanism of GP extracts and its fraction, HH-F3. Results: We demonstrated that GP extracts and HH-F3 downregulated the expression levels of extracellular matrix (ECM) proteins and inhibited the proliferation and migration via suppression of the TGF-β1 pathway in rat hepatic stellate HSC-T6 cells. Moreover, the HH-F3 fraction decreased hepatic collagen content and reduced plasma AST, ALT, and γ-GT activities in a DEN-induced rat liver injury model, suggesting that GP/HH-F3 has hepatoprotective effects against DEN-induced liver fibrosis. Conclusion: These findings indicate that GP/HH-F3 may be a potential therapeutic agent for the treatment of liver fibrosis. The inhibition of TGF-β-mediated fibrogenesis may be a central mechanism by which GP/HH-F3 protects the liver from injury.

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