Quantitative analysis of regenerating and degenerating areas within the lobule of the carbon tetrachloride-injured liver

Morrison, George R.; Brock, Frances E.; Karl, Irene E.; Shank, Robert E.

doi:10.1016/0003-9861(65)90208-0

Cited by 84 publications

(32 citation statements)

References 20 publications

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“…These free radicals contribute to lipid peroxidation that disrupts calcium homeostasis, gradually leading to the necrosis of hepatocytes and cell membrane injury surrounding the central vein. Finally, the necrosis of hepatocytes and hypo-immunity result in liver injury (Morrison et al 1965;Xu and Qu 2008;Bockhold et al 2005;Fausto 2006 (Wang et al 2011;Sun et al 2008). MDA is the end product in the lipid peroxidation, so measuring the concentration of MDA in the liver can indicate the extent of damage of hepatic cells indirectly (Li et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

et al. 2016

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Human umbilical cord mesenchymal stem cells (hUMSCs) have been shown to have multiple differentiation potentials. However, a key problem is that only a small number of hUMSCs can migrate to damaged tissue after transplantation. According to ''The Theory of Kidney Essence'' in Traditional Chinese Medicine, some traditional Chinese medicines used for tonifying the kidneys can be applied in promoting the differentiation and migration of stem cells in vivo. Our previous study demonstrated that icariin (ICA) could up-regulate the pluripotent genes of hUMSCs in vitro and induce cell migration in mice in an acute kidney injury model in vivo. The aim of this study was to investigate the effects of ICAinduced hUMSCs in chronic liver injury (CLI) caused by carbon tetrachloride (CCl 4 ). CLI was induced by intraperitoneal injection of CCl 4 . ICA-treated hUMSCs were transplanted via intra-venous injection. The animals were followed for survival, biochemistry analysis and pathology. The results show that ICAtreated hUMSCs accelerate the recovery of liver function in mice with CLI. In addition, ICA-treated hUMSCs increase the anti-oxidant activities in liver and prevent the progression to hepatic fibrosis. Moreover, ICA induces the migration of hUMSCs to the injured liver tissue. In conclusion, these data demonstrate that ICA-treated hUMSCs exhibit recovery and protective properties in the mice model of CCl 4 -induced CLI.

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Section: Discussionmentioning

confidence: 99%

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

et al. 2016

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“…The dehydrogenase activities were determined fluorimetrically in tissue samples of 100 -600 ng dry weight or equivalent amounts of homogenate. 3-HydroxyacylCoA dehydrogenase was tested at 25°C in 1Opl of the following test solution modified according to [21] : 0.3 mM NADH, 0.4 mM acetoacetyl-CoA, 2 mM amytal, 1 mM nicotinamide, 2 mg/ml bovine serum albumin in 50 mM sodium pyrophosphate buffer, pH 6.4. The reaction was stopped after 5 min by addition of 10 p150 mM HC1, followed by incubation at 40 "C for 15 min, in order to destroy any remaining NADH.…”

Section: Microussaysmentioning

confidence: 99%

Distribution of enzymes of fatty acid and ketone body metabolism in periportal and perivenous rat‐liver tissue

Katz

Fischer

Giffhorn

1983

European Journal of Biochemistry

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The zonal distribution of cytosolic acetyl-CoA carboxylase, mitochondria1 3-hydroxyacyl-CoA dehydrogenase and 3-hydroxybutyrate dehydrogenase was studied in microdissected liver tissue.1. In fed male and female rats the activity of the lipogenic enzyme acetyl-CoA carboxylase was 1.6-times higher in the perivenous than in the periportal zone of the liver acinus.2.3-Hydroxybutyrate dehydrogenase, which is involved in the formation of the ketone body, 3-hydroxybutyrate, exhibited a similar distribution pattern with a 1.5-1 %times higher activity in the perivenous than in the periportal zone.3. In contrast, the activity of 3-hydroxyacyl-CoA dehydrogenase, the third enzyme in 6-oxidation, was about equally distributed between the periportal and the perivenous zone of the liver acinus.The results indicate a predominance of lipogenesis in the perivenous, mainly glycolytic zone of the liver acinus.Furthermore, these data support the hypothesis that P-oxidation supplies energy for basic and anabolic processes like gluconeogenesis in the periportal zone, while it provides acetyl-CoA for ketogenesis besides energy for basic needs in the perivenous zone.

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“…16,17 Carbon tetrachloride liver injury causes necrosis of hepatocytes surrounding the central vein caused by local expression of a P450 enzyme forming toxic free radical metabolites. 18 Following removal of the pericentral necrotic tissue by inflammatory cells, they are replaced by replicating periportal hepatocytes. 18 Furthermore, hepatic repair following CCl 4 injury involves a transient differentiation of stellate cells into fibrogenic myofibroblasts (activation), which secrete collagen that is essential for reestablishment of normal liver architecture.…”

mentioning

confidence: 99%

“…18 Following removal of the pericentral necrotic tissue by inflammatory cells, they are replaced by replicating periportal hepatocytes. 18 Furthermore, hepatic repair following CCl 4 injury involves a transient differentiation of stellate cells into fibrogenic myofibroblasts (activation), which secrete collagen that is essential for reestablishment of normal liver architecture. 19 Chronic liver injury and repair results in massive proliferation of activated stellate cells, causing hepatic fibrosis and cirrhosis, thereby disrupting hepatic regeneration and leading to liver failure.…”

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confidence: 99%

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

et al. 2003

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Previous studies have shown that haploinsufficiency of the splanchnic and septum transversum mesoderm Forkhead Box (Fox) f1 transcriptional factor caused defects in lung and gallbladder development and that Foxf1 heterozygous (؉/؊) mice exhibited defective lung repair in response to injury. In this study, we show that Foxf1 is expressed in hepatic stellate cells in developing and adult liver, suggesting that a subset of stellate cells originates from septum transversum mesenchyme during mouse embryonic development. Because liver regeneration requires a transient differentiation of stellate cells into myofibroblasts, which secrete type I collagen into the extracellular matrix, we examined Foxf1 ؉/؊ liver repair following carbon tetrachloride injury, a known model for stellate cell activation. We found that regenerating Foxf1 ؉/؊ liver exhibited defective stellate cell activation following CCl 4 liver injury, which was associated with diminished induction of type I collagen, ␣-smooth muscle actin, and Notch-2 protein and resulted in severe hepatic apoptosis despite normal cellular proliferation rates. Furthermore, regenerating Foxf1 ؉/؊ livers exhibited decreased levels of interferon-inducible protein 10 (IP-10), delayed induction of monocyte chemoattractant protein 1 (MCP-1) levels, and aberrantly elevated expression of transforming growth factor ␤1. T he Forkhead Box (Fox) family of transcription factors shares homology in the winged helix DNA binding domain, 1 and its members play important roles in cellular proliferation, differentiation, and metabolic homeostasis. [2][3][4][5][6] Haploinsufficiency of the Foxf1 gene (previously known as HFH-8 or Freac-1) in heterozygous (ϩ/Ϫ) mice causes perinatal lethality from pulmonary hemorrhage and severe defects in alveolarization, vascularization, and fusion of lung lobes. 7-9 Lung hemorrhage was observed in one half of newborn Foxf1 ϩ/Ϫ mice that had an 80% reduction in pulmonary Foxf1 levels (low Foxf1 ϩ/Ϫ) and reduced expression of genes involved in lung morphogenesis. 7 Interestingly, expression of these lung developmental genes was unchanged in 40% of the newborn Foxf1 ϩ/Ϫ mice that had near wildtype (WT) pulmonary levels of Foxf1 messenger RNA (mRNA) (high Foxf1 ϩ/Ϫ mice) without pulmonary hemorrhage, but they exhibited diminished alveolar septation. 7 Moreover, the high Foxf1 ϩ/Ϫ mice had normal life spans and adult lung morphology, suggesting that these mice compensated for the alveolar septation defect but exhibited defective lung repair in response to injury. 10 Liver development initiates at 9 days postcoitum (dpc) of mouse embryogenesis, when the cardiac mesenchyme induces the hepatic primordium to emerge from the foregut endoderm that invades the septum transversum mesenchyme. 6 Previous expression studies have shown

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Quantitative analysis of regenerating and degenerating areas within the lobule of the carbon tetrachloride-injured liver

Cited by 84 publications

References 20 publications

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

Distribution of enzymes of fatty acid and ketone body metabolism in periportal and perivenous rat‐liver tissue

Foxf1 +/− mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury

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