epidermal-growth-factor and Carbon-Tetrachloride-Poisoning

epidermal-growth-factor has been researched along with Carbon-Tetrachloride-Poisoning* in 6 studies

Other Studies

6 other study(ies) available for epidermal-growth-factor and Carbon-Tetrachloride-Poisoning

ArticleYear
Effect of IL-10 on the expression of HSC growth factors in hepatic fibrosis rat.
    World journal of gastroenterology, 2005, Aug-21, Volume: 11, Issue:31

    To study the effect of IL-10 on the expression of growth factors--transforming growth factor-beta1 (TGF-beta1), epidermal growth factor (EGF), hepatocyte growth factor (HGF) and platelet-derived growth factor (PDGF) of hepatic stellate cells (HSCs) of hepatic fibrosis rat and the anti-fibrogenic role of exogenous IL-10.. Hepatic fibrosis was induced by CCl(4) administration intra-peritoneally. Sixty clean male Sprague-Dawley (SD) rats were randomly divided into three groups: normal control group (GN, 8 rats), hepatic fibrosis model group (GC, 28 rats) and IL-10 treated group (GI, 24 rats). At the beginning of the 7th and 11th wk, rats in each group were routinely perfused with pronase E and type IV collagenase through a portal vein catheter and the suspension obtained from the liver was spun by centrifugation with 11% Nycodenz density gradient to isolate HSCs. Histological examination was used to determine the degree of hepatic fibrosis. RT-PCR was employed to analyze mRNA expression from freshly isolated cells. Immunocytochemistry was performed to detect protein expression in primary cultured HSCs.. Rat hepatic fibrosis was developed with the increase of injection frequency of CCl(4), and HSCs were successfully isolated. At the 7th and 11th wk, TGF-beta1, EGF, and HGF mRNA in GC increased obviously compared with GN (P = 0.001/0.042, 0.001/0.001, 0.001/0.001) and GI (P = 0.001/0.007, 0.002/0.001, 0.001/0.001). For TGF-beta1, no difference was observed between GI and GN. For EGF, mRNA level in GI increased compared with GN during the 7th wk (P = 0.005) and 11th wk (P = 0.049). For HGF, mRNA level in GI decreased compared with GN at the 7th wk (P = 0.001) and 11th wk (P = 0.021). Between these two time points, TGF-beta1 expression at the 7th wk was higher than that of the 11th wk (P = 0.049), but for EGF, the former was lower than the latter (P = 0.022). As for PDGF mRNA, there was no significant difference between these groups, but difference seemed to exist in protein levels. Results by immunocytochemistry of TGF-beta1 and EGF were paralleled with the above findings.. The expression of TGF-beta1, EGF and HGF increased in HSC of hepatic fibrosis rat and decreased after treatment with IL-10. IL-10 plays an anti-fibrogenic role by suppressing growth factors expression.

    Topics: Animals; Base Sequence; Carbon Tetrachloride Poisoning; DNA Primers; Epidermal Growth Factor; Gene Expression Regulation; Hepatocyte Growth Factor; Interleukin-10; Liver Diseases; Male; Rats; Rats, Sprague-Dawley; RNA, Messenger; Transforming Growth Factor beta; Transforming Growth Factor beta1

2005
Epidermal growth factor protects against carbon tetrachloride-induced hepatic injury.
    Clinical science (London, England : 1979), 1998, Volume: 94, Issue:3

    1. Epidermal growth factor (EGF) is known to protect the gastrointestinal tract against various noxious agents. Its potential value in preventing/ treating hepatic injury is, however, largely unexplored. We therefore examined whether EGF could influence CCl4-induced hepatic injury. 2. Female Sprague-Dawley rats (8 per group) received saline or recombinant EGF (500 or 750 micrograms/kg, intraperitoneal) 30 min before CCl4 (20% v/v, in olive oil, intraperitoneal). Eighteen hours later, animals were killed, serum was collected for assay of biochemical markers of hepatic injury and livers were removed for histological analyses. 3. Administration of CCl4 resulted in severe hepatic necrosis and caused a 10-fold rise in plasma alanine aminotransferase levels compared with levels seen in control animals (218 +/- 15 compared with 23 +/- 9 mumol/l in controls, mean +/- SEM, P < 0.01). Serum malondialdehyde levels, used as a marker of lipid peroxidation, showed a 2-fold rise in response to CCl4 treatment (median 4.0, quartile range 3.3-5.8 units/l compared with median 2.3, quartile range 2.1-2.5 units/l in controls, P < 0.05). Administration of EGF at 500 micrograms/kg, before the CCl4, did not protect against injury, as assessed by histology or rise in plasma alanine aminotransferase levels. In contrast, animals given EGF at 750 micrograms/kg, before the CCl4, had only minimal changes in histology, with only a minor rise in alanine aminotransferase levels (37 +/- 4 compared with 23 +/- 9 mumol/l in animals not given CCl4) and had no significant rise in malondialdehyde levels. 4. EGF protects against CCl4-induced hepatic injury and may provide a novel approach to the treatment of liver damage.

    Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cytoprotection; Dose-Response Relationship, Drug; Epidermal Growth Factor; Female; Liver; Necrosis; Rats; Rats, Sprague-Dawley; Recombinant Proteins

1998
Effect of epidermal growth factor on cultured rat hepatocytes poisoned by CCl4.
    Zhongguo yao li xue bao = Acta pharmacologica Sinica, 1997, Volume: 18, Issue:2

    To study the effects of epidermal growth factor (EGF) on CCl4-induced primary cultured hepatocytes injury.. Alanine amino-transferase (AlaAT) and aspartate aminotransferase (AspAT) activities and K+ concentractions were determined by the Auto-biochemistry Assay System. Malondialdehyde (MDA) was determined by thiobarbituric acid method. Radioactivity was determined by liquid scintillometry. Light microscopy and electron microscopy were used.. EGF 40 micrograms.L-1 decreased CCl4 (10 mmol.L-1)-induced damages of rat primary cultured hepatocytes by decreasing AlaAT and AspAT leakage and MDA production, and promoted RNA and DNA synthesis, with a high positive correlation between intracellular K+ leakage and DNA syntheses (r = 0.99, P < 0.01). Cytopathological study showed that EGF decreased damage of liver cells.. EGF maintains the stability of cellular lipid membrane and promotes syntheses of RNA and DNA of hepatocytes, and intracellular K+ transference is a promotor of the message transmission of DNA synthesis.

    Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Cells, Cultured; DNA; Epidermal Growth Factor; Female; Liver; Male; Malondialdehyde; Rats; Rats, Sprague-Dawley; RNA

1997
Heterogeneous activation of protein kinase C during rat liver regeneration.
    Advances in second messenger and phosphoprotein research, 1990, Volume: 24

    Topics: Animals; Carbon Tetrachloride Poisoning; Cells, Cultured; Chemical and Drug Induced Liver Injury; DNA Replication; Enzyme Activation; Epidermal Growth Factor; Insulin; Isoenzymes; Liver; Liver Regeneration; Protein Kinase C; Proto-Oncogene Proteins c-myc; Rats

1990
[Studies on metabolic characteristics of cirrhotic rat hepatocytes using primary culture].
    Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 1990, Volume: 87, Issue:6

    To assess the metabolic characteristics of cirrhotic hepatocytes, a primary culture of hepatocytes was established using rat liver induced cirrhosis by CCl4 administration. Using this system, cell responsiveness to different metabolic and excretory stimuli was investigated and compared with a primary culture of normal healthy rat hepatocytes. Cirrhotic hepatocytes showed reduced protein synthesis in response to insulin and reduced urea synthesis in response to glucagon. However, DNA synthesis stimulated by insulin and EGF was significantly enhanced in cirrhotic hepatocytes. No significant difference was observed in the fluorescein diacetate excretion rate. Cirrhotic hepatocytes showed impairment of antipyrine metabolism and conjugation and excretion of unconjugated bilirubin. These results suggest indirectly that cirrhotic hepatocytes may be less functionally mature than normal healthy hepatocytes.

    Topics: Animals; Antipyrine; Carbon Tetrachloride Poisoning; Cells, Cultured; DNA; Epidermal Growth Factor; Fluoresceins; Glucagon; Insulin; Liver; Liver Cirrhosis, Experimental; Male; Rats; Rats, Inbred Strains; Urea

1990
Alterations in the functional expression of receptors on cirrhotic rat hepatocytes.
    Hepatology (Baltimore, Md.), 1989, Volume: 9, Issue:1

    Reduced hepatic uptake and clearance of macromolecules in liver cirrhosis is due to two major factors: increased diffusional barriers, resulting primarily from the deposition of excessive connective tissue in the space of Disse, and hepatocellular dysfunction, manifested by receptor and/or postreceptor defects. To probe the mechanisms underlying hepatocellular dysfunction in liver cirrhosis, we have investigated receptor-ligand interactions for asialoorosomucoid, insulin and epidermal growth factor in hepatocytes isolated from the livers of rats chronically exposed to phenobarbital and carbon tetrachloride for up to 12 weeks. Viable cells were allowed to attach at 37 degrees C and the high-affinity cell surface binding sites for each ligand were assessed at 4 degrees C in the presence of [125I]-ligand. In parallel incubations, digitonin (0.055%) was added to the binding medium to assess total cellular binding sites. Results demonstrated that chronic treatment of rats with phenobarbital increased hepatocyte asialoorosomucoid surface receptor affinity (p less than 0.05) but had no affect on the number of asialoglycoprotein binding sites. Treatment with CCl4 and phenobarbital significantly reduced the number of surface binding sites for asialoorosomucoid (p less than 0.05) and epidermal growth factor (p less than 0.02), although this treatment had no effect on either the binding affinity or the number of binding sites for insulin. The decrease in cell surface binding sites for asialoorosomucoid and epidermal growth factor was not due to a redistribution of the surface sites to intracellular locations, since the total number of cellular binding sites also was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Animals; Asialoglycoprotein Receptor; Carbon Tetrachloride Poisoning; Epidermal Growth Factor; ErbB Receptors; Insulin; Liver Cirrhosis, Experimental; Male; Phenobarbital; Rats; Rats, Inbred Strains; Receptor, Insulin; Receptors, Cell Surface; Receptors, Immunologic

1989
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