Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that supplemental vitamin E has a cytoprotective effect in the liver of rats with chronic CCL4-induced liver cirrhosis. In this study, we hypothesized that vitamin E would have a protective effect in acute liver injury induced by D-galactosamine. D-Galactosamine-induced injury has been thought to be due to a synergistic direct toxic effect and presence of intestinal bacteria and/or endotoxins. D-Galactosamine was used to induce acute "hepatitis" (1.5-2.0 g/Kg body weight, ip). Rats were placed on either standard chow or the same chow supplemented with vitamin E (300 mg DL-alpha-tocopherol/Kg diet) and 6 days later were given D-galactosamine. There was significantly improved early (5-day) survival and late (14-day) survival in the vitamin E-supplemented group. The vitamin E beneficial effect was manifested also by decreased liver fat and collagen content and decreased SGPT level. Because bacterial endotoxins have been implicated as playing a role in the pathogenesis of D-galactosamine hepatitis, the same experiment was carried out using germ-free and conventional rats. There was significantly improved survival in both the germ-free and conventional vitamin E-supplemented groups both at 5 and 14 days. There was no significant difference between conventional and germ-free rats with or without vitamin E supplementation. In summary (a) vitamin E improves the early fat and collagen accumulation in the liver, decreases SGPT level, and improves survival in the D-galactosamine experimental model of acute liver injury in both conventional and germ-free rats; and (b) D-galactosamine toxicity is probably not mediated through intestinal bacteria and/or endotoxins.
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PMID:Protective effect of vitamin E in rats with acute liver injury. 395 25

Preclinical animal models allow to study development and progression of several diseases, including liver disorders. These studies, for ethical reasons and medical limits, are impossible to carry out in human patients. At the same time, such experimental models constitute an important source of knowledge on pathomechanisms for drug- and virus-induced hepatotoxicity, both acute and chronic. Carbon tetrachloride, D-Galactosamine, and retrorsine are xenobiotics that can be used in immunocompetent animal models of hepatotoxicity, where chemical-intoxicated livers present histological features representative of human viruses-related infection. A prolonged derangement into liver architecture and functions commonly lead to cirrhosis, eventually resulting in hepatocellular carcinoma. In human, orthotopic liver transplantation commonly resolve most the problems related to cirrhosis. However, the shortage of donors does not allow all the patients in the waiting list to receive an organ on time. A promising alternative treatment for acute and chronic liver disease has been advised in liver cell transplantation, but the limited availability of hepatocytes for clinical approaches, in addition to the immunosuppressant regiment required to sustain cellular long-term engraftment have been encouraging the use of alternative cell sources. A recent effective source of stem cells have been recently identified in the human amnion membrane. Human amnion epithelial cells (hAEC) have been preclinically tested and proven sufficient to rescue immunocompetent rodents lethally intoxicated with drugs. The adoption of therapeutic procedures based on hAEC transplant in immunocompetent recipients affected by liver diseases, as well as patients with immune-related disorders, may constitute a successful new alternative therapy in regenerative medicine.
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PMID:Assessment of animal experimental models of toxic liver injury in the context of their potential application as preclinical models for cell therapy. 3140 48