transforming-growth-factor-alpha and Carbon-Tetrachloride-Poisoning
transforming-growth-factor-alpha has been researched along with Carbon-Tetrachloride-Poisoning* in 3 studies
Other Studies
3 other study(ies) available for transforming-growth-factor-alpha and Carbon-Tetrachloride-Poisoning
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Protective mechanism of Lygodium flexuosum extract in treating and preventing carbon tetrachloride induced hepatic fibrosis in rats.
The protective effect of Lygodium flexuosum extract in preventive and curative treatments of CCl(4) induced fibrosis was quantified. Hepatic fibrosis was induced in male Wistar rats by CCl(4) administration (150 microL/100 gm rat weight, oral) twice a week for 10 weeks. In preventive treatment daily doses of L. flexuosum n-hexane extract (200 mg/kg, p.o) were administered for 10 weeks. In curative treatment L. flexuosum extract (200 mg/kg, p.o) was given for 2 weeks after the establishment of fibrosis for 10 weeks. Treatment with the n-hexane extract (200 mg/kg) reduced the mRNA levels of proinflammatory cytokines, growth factors and other signaling molecules, which are involved in hepatic fibrosis. The expression levels of tumor necrosis factor-alpha, interleukin-1beta, transforming growth factor-beta1, procollagen-I, procollagen-III and tissue inhibitor of metalloproteinase-1 were elevated during carbon tetrachloride administration and reduced the levels to normal by the treatment with the extract treatment. The increased levels of matrix metalloproteinase-13 in extract treated rats were indicative of the protective action of L. flexuosum n-hexane extract. In conclusion, L. flexuosum n-hexane extract functions as a potent fibrosuppresant, effectively reverses carbon tetrachloride-induced hepatic fibrosis in curative treatment and reduces the effects of ongoing toxic liver injury in preventive treatment by promoting extracellular matrix degradation in the fibrotic liver. Topics: Animals; Antineoplastic Agents, Phytogenic; Carbon Tetrachloride Poisoning; Ferns; Liver Cirrhosis; Male; Matrix Metalloproteinase 13; Plant Extracts; Procollagen; Protective Agents; Rats; Rats, Wistar; Tissue Inhibitor of Metalloproteinase-1; Transforming Growth Factor alpha; Transforming Growth Factor beta1 | 2007 |
Acute liver CCl(4) intoxication causes low HSP70 gene expression and a delayed transition through the cell cycle in aged rats.
Since there is still debate about the ability of the aged liver to regenerate, we compared some aspects of this response in young, adult and old rodents. 2, 6, 12 and 19-month-old rats were intraperitoneally injected with CCl(4) (3mg/kg) or left untreated (CT) and killed either 2h (group A) or 24h (group B) after intoxication. Liver injury was checked histologically and by assaying transaminases. mRNA levels of albumin (Alb), c-fos, c-myc, hepatocyte growth factor (HGF), transforming growth factor (TGF)-alpha and TGF-beta1 were also analyzed. Heat shock protein (HSP)70 gene expression was evaluated, and liver GSH content. Transaminases and histology show more damage in aged rats. Alb mRNA was reduced starting at 12 months in group A and at all ages in group B; c-fos and c-myc mRNAs reached the highest levels in 6-month-old rats and the lowest in those aged 12 and 19 months of group A. In group B, c-fos was detectable only in 6-month animals, but c-myc at all ages. HGF, TGF-alpha and TGF-beta1 mRNAs were up-regulated in treated rats, but to a lesser extent in the aged. HSP70 mRNA, absent in CT, was significantly increased at the age of 6 months, undetectable in the oldest rats in group A; in group B it was only visible in 6-month animals. GSH content was reduced with aging. In conclusion, during aging the liver regenerative machinery is preserved but its activation is reduced and delayed. Topics: Aging; Alanine Transaminase; Albumins; Animals; Aspartate Aminotransferases; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Cell Cycle; Gene Expression; Glutathione; Hepatocyte Growth Factor; HSP70 Heat-Shock Proteins; Liver; Male; Proto-Oncogene Proteins c-fos; Proto-Oncogene Proteins c-myc; Rats; Rats, Sprague-Dawley; Transforming Growth Factor alpha; Transforming Growth Factor beta; Transforming Growth Factor beta1 | 2002 |
Age-related differences in TGF-alpha and proto-oncogenes expression in rat liver after a low dose of carbon tetrachloride.
The resiliency of rats during early post-natal development to CCl4 or to an interactive hepatotoxicity of chlordecone (CD) + CCl4 has been shown to be due to an efficient stimulation of tissue repair. The objective of the current study was to investigate if this is due to efficient expression of transforming growth factor-alpha (TGF-alpha) and proto-oncogenes. Postnatally developing (20 day old) and adult (60 day old) male Sprague-Dawley rats were challenged with a single low dose of CCl4 (100 microL/kg, ip) or corn oil. Liver samples were collected during a time course (0-96 h) after the administration of CCl4 and used to examine TGF-alpha and early (c-fos) and late (H-ras and K-ras) proto-oncogenes mRNA expressions. Significant increases in TGF-alpha, H-ras, and K-ras gene expressions were evident as early as 12 hours after CCl4 and peaked between 24 and 48 hours in an age-dependent manner as detected by slot-blot analysis. Results of the study revealed three- and twofold increases in TGF-alpha gene expression in 20 and 60 day old rats, respectively, after CCl4. There were 3.5- and 2.5-fold increases in H-ras and 4.4- and 3.4-fold increases in K-ras in 20 and 60 day old rats, respectively. In contrast, a 10-fold increase in c-fos mRNA expression was evident in 20 day old rats 1 hour after CCl4 treatment, returning to the baseline value by 3 hours, whereas in 60 day old rats, this increase was less than twofold. The overall findings of this study indicate that TGF-alpha and the early and late proto-oncogene mRNA expressions were enhanced in an age- and time-dependent manner in response to a low dose of CCl4. These results further strengthen the view that the remarkable resiliency of rats to hepatotoxicants during early postnatal development is due to substantial increases in stimulation of hepatocellular regeneration and tissue repair mechanisms, leading to regression of liver injury and recovery. Topics: Aging; Animals; Carbon Tetrachloride Poisoning; Gene Expression; Genes, ras; Immunoblotting; Liver; Liver Regeneration; Male; Poly A; Proto-Oncogene Proteins c-fos; Proto-Oncogenes; Rats; Rats, Sprague-Dawley; RNA, Messenger; Transforming Growth Factor alpha | 1995 |