Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

'Arogyavardhini'-an indigenous formulation was evaluated for its hepatoprotective activity in rats, using two models of carbon tetrachloride (CCl4) hepatic damage, one simulating vital hepatitis and the other simulating fatty change. The protective effect was assessed from serum aspartate transaminase (AST) and alkaline phosphatase levels and from histopathological changes in liver. The results revealed that 'Arogyavardhini' (5 mg/100g, PO daily) was effective in minimizing the changes in serum levels of AST and alkaline phosphatase induced by CCI. The protective effect was also evident on histopathological examination.
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PMID:Effect of 'Arogyavardhini' against carbon tetrachloride induced hepatic damage in albino rats. 366 71

High levels of acute phase proteins (acute phase reactants, APR) suppress acute inflammatory reactions in the rat. As many APR have antiprotease properties, including an anticollagenase activity, the effect of APR on the development of CCl4-induced liver fibrosis was investigated in rats. APR were provoked by repeated injections of epinephrine, inducing a broad spectrum of APR. This reaction can be monitored measuring alpha 2-macroglobulin levels in the rat (alpha 2-macrofetoprotein, alpha M FP). This protein was found to inhibit both acute galactosamine hepatitis and acute CCl4-induced liver toxicity. The animals with high levels of APR at the start of CCl4 treatment developed a more severe degree of fibrosis and cirrhosis than the control group in which no acute phase reaction was induced. Epinephrine alone had no such effects. Additionally, the APR positive group showed an initially lower degree of hepatocellular damage when compared to control animals. This uncoupling of liver cell damage and subsequent fibrosis may demonstrate that higher levels of APR might be important as to the development of cirrhosis, possibly based on the anticollagenase activity of these proteins.
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PMID:Acute phase reactants enhance CCl4 induced liver cirrhosis in the rat. 369 34

Phospholipid composition and oxidative phosphorylation were studied in liver mitochondria of rats with experimental chronic hepatitis. The hepatitis was simulated by means of two hepatotropic drugs--heliotrin and CCl4. Content of phosphatidyl inositol was decreased and that of phosphatidic acid--increased in the hepatitis independently of the nature of the agent inducing the disease. At the same time, content of lysophosphatidyl ethanolamine was decreased but content of lysocardiolipine and lysophosphatidic acid was increased. In CCl4-induced hepatitis content of cardiolipine and sphingomyelin was decreased, whereas after the treatment with heliotrin content of cardiolipine in liver tissue was unaltered and that of sphingomyelin was increased. Content of lysophosphatidyl choline was considerably increased in CCl4-hepatitis but it was only slightly altered after the treatment with heliotrin. The most pronounced alterations in the phospholipid spectrum and oxidative phosphorylation were found in liver mitochondria in the CCl4-induced hepatitis.
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PMID:[Phospholipid composition and oxidative phosphorylation in liver mitochondria in hepatitis]. 372 68

Level of fructose-1-monophosphate aldolase was decreased in blood serum after administration of phosphatidyl choline-containing liposomes into male rats with experimental toxic hepatitis caused by treatment with hepatotropic poison CCl4 at a dose of 0.25 ml/100 g of body mass. The rate of the aldolase level normalization depends on composition of liposomes as well as on the pathway of their administration.
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PMID:[Protective effect of phosphatidylcholine liposomes in experimental toxic hepatitis]. 372 72

Suramin that accumulates in rat liver Kupffer cell lysosomes and inhibits the intralysosomal proteolysis was used to suppress the functional activity of these particles during liver damage (acute CCl4 hepatitis). Polyvinylpyrrolidone that does not disturb protein catabolism in liver lysosomes was employed for reference. According to the characteristic changes in lysosomes induced by suramin (inhibition of acid phosphatase, decrease of the rate of the intralysosomal proteolysis in the liver) and PVP the damaged liver was able to accumulate the lysosomotropic substances under study. Suramin aggravated liver damage and increased the lysosomal labilization, whereas PVP exhibited the protective action. The unfavourable effect of suramin may be linked with the suppression of catabolism of Kupffer cell lysosomes. The data obtained suggest the lack of safety of using the inhibitors of intralysosomal proteolysis in patients with acute hepatitis.
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PMID:[Facilitation of the structural and functional disorders of liver lysosomes in toxic hepatitis due to the suppression of intralysosomal proteolysis]. 389 40

After administration of phytoecdisteroids (ecdisterone, turkesterone) at a dose of 5 mg/kg and the anabolic steroid preparation nerobol at a dose of 10 mg/kg into rats with experimental hepatitis caused by CCl4 poisoning, positive alterations were found in activity of the polyenzymatic systems in membranes of liver mitochondria simultaneously with an increase in their stability and resistance to the effect of exogenous factors producing the mitochondria degradation (controlled heating, treatment with phospholipase A2 or trypsin). These alterations, which appear to occur due to development of strong binds between phospholipids and proteins of inner mitochondrial membrane, promoted normalization of the respiratory chain and the outer pathway of electron transport in hepatocytes of rats with hepatitis.
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PMID:[Effect of phytoecdysteroids and steranobols on the activity and stability of membrane-bound enzymes of liver mitochondria in experimental hepatitis]. 395 17

The chronic course of viral and toxic hepatitis is associated with the involvement into the pathogenesis of the disease of the immune processes whose mechanisms remain obscure. An attempt was made to elucidate the localization of immune complexes in the liver of rats with CCl4-induced cirrhosis of the liver according to the method by Yu. F. Kubitsa. Immune complexes were found in macrophages and lymphocytes infiltrating perivascular spaces and walls of veins undergoing degeneration. This indicates a possible role of cell-mediated reactions in the damage of blood vessels and hepatic parenchyma in cirrhosis. Immune complexes wee also found in the hepatocyte nuclei which suggests a damaging effect of antibody on the hepatic tissue in cases of complement activation.
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PMID:[Localization of immune complexes in the liver in experimental cirrhosis]. 645 75

In experimental toxic hepatitis induced by injection of CCl4 into rats, the rat blood and urine content of acetylated sulfamonomethoxine diminishes, the acetylation of sulfamonomethoxine and norsulfazole in an isolated stomach of the rat reduces, and acetylation of sulfamonomethoxine is inhibited by rat liver and small intestine homogenates. This confirms that different types of pathology (infectious and non-infectious) provoke the same line of changes, namely the reduction of acetylation of sulfanilamide substances in the body. CCl1 decreases sulfamonomethoxine acetylation by a mixture of the mitochondria and microsomes of the rat liver, i. e. eliminates the synergistic effect characteristic for intact rats. The reduction of acetylation recorded at different levels of the organization of the living systems--bodily, organ and subcellular ones--is accounted for by the lowering of the acetylcoenzyme A content in the tissues. One of the reasons for reduction of acetylation during the CCl4-induced liver injury lies in the impairment in the liver cells of the interaction between the mitochondria and endoplasmic reticulum.
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PMID:[Acetylation of sulfanilamide substances in toxic lesions of the liver]. 650 37

The accelerated transport of the blood neutral amino acids into the brain in encephalopathic patients with fulminant hepatitis and advanced liver cirrhosis was demonstrated not only by determining the cerebrospinal fluid (CSF) aminogram but also by calculating the predicted velocity of the amino acid transport through the blood-brain barrier. Significant elevation in CSF aromatic amino acid (AAA) and methionine levels was observed in the encephalopathic patients. Arousal from hepatic encephalopathy by drip infusion of a branched chain amino acid (BCAA)-enriched solution was obtained coincidentally with the elevated BCAA levels and diminished concentrations of AAA and methionine in CSF. These clinical observations were confirmed experimentally in rats treated with carbon tetrachloride (CCl4) and D-galactosamine by obtaining the elevation of neutral amino acid contents in the brain and the slight increase in the brain uptake index (BUI) of a radiolabeled amino acid.
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PMID:Alterations in neutral amino acid transport across the blood-brain barrier in hepatic failure. 663 35

Antitoxic properties of cobamamide, a coenzymic form of vitamin B12, were studied in experimental toxic hepatitis induced by CCl4. The data obtained as a result of the assessment of the bromosulfalene test and activity of sorbitol dehydrogenase and alanine aminotransferase point to a demonstrable hepatoprotective action of cobamamide. Normalization of the indicators studied evidences that the drug intensifies the recovery processes occurring in the liver of rabbits with toxic hepatitis.
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PMID:[Antitoxic action of cobamamide in experimental hepatitis]. 673 13


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