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Cholesterol-induced stimulation of postinflammatory liver fibrosis.

https://arctichealth.org/en/permalink/ahliterature90629
Source
Bull Exp Biol Med. 2008 Jun;145(6):692-5
Publication Type
Article
Date
Jun-2008
Author
Schwartz Y Sh
Dushkin M I
Komarova N I
Vorontsova E V
Kuznetsova I S
Author Affiliation
Institute of Therapy, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. Russia. yshschwartz@mail.ru
Source
Bull Exp Biol Med. 2008 Jun;145(6):692-5
Date
Jun-2008
Language
English
Publication Type
Article
Keywords
Animals
Calcitriol - pharmacology
Cholesterol Esters - metabolism
Cholesterol, Dietary - administration & dosage
Collagen - metabolism
Gene Expression - drug effects
Heptanoic Acids - pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Liver - drug effects - metabolism - pathology
Liver Cirrhosis - etiology - metabolism - prevention & control
Male
Mevalonic Acid - pharmacology
Mice
Mice, Inbred C57BL
Pyrroles - pharmacology
Transforming Growth Factor beta1 - genetics
Triglycerides - metabolism
Zymosan - pharmacology
Abstract
We studied the effect of high-cholesterol diet and factors inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase on the development of liver fibrosis in C57Bl/6 mice with CCl4- or zymosan-induced hepatitis. Feeding a high-cholesterol diet led to a sharp increase in collagen content in the liver tissue of animals with CCl4-induced or zymosan-induced hepatitis. Atorvastatin and calcitriol produced less pronounced fibrogenic effects. Mevalonate partially prevented the development of cholesterol-induced fibrogenesis. High-cholesterol diet led to accumulation of oxysterols, cholesterol esters, and triglycerides and increased the expression of transforming growth factor-beta1 mRNA in liver tissue. Cholesterol-induced potentiation of the fibrogenic response is probably associated with transforming growth factor-beta1 induction due to accumulation of lipids and oxysterols in the liver.
PubMed ID
19110552 View in PubMed
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[Effect of stimulation and inhibition of macrophage functions on hypercholesterolemia in rats]

https://arctichealth.org/en/permalink/ahliterature45980
Source
Vopr Med Khim. 2002 Mar-Apr;48(2):180-8
Publication Type
Article
Author
P O Kuznetsov
A F Safina
Ia Sh Shvarts
D D Tsyrendorzhiev
A A Zubakhin
M I Dushkin
Author Affiliation
Institute of Internal Medicine, Siberian Division of the Russian Academy of Medical Sciences, Vladimirovski st. 2a, Novosibirsk 630003, Russia.
Source
Vopr Med Khim. 2002 Mar-Apr;48(2):180-8
Language
Russian
Publication Type
Article
Keywords
Animals
Bile Acids and Salts - metabolism
Biological Transport
Cholesterol - blood - metabolism
Cholesterol Esterase - metabolism
Cholesterol Esters - blood
Depression, Chemical
English Abstract
Gadolinium - pharmacology
Hypercholesterolemia - chemically induced - metabolism
Kupffer Cells - drug effects - pathology
Lipoproteins, LDL - blood
Lipoproteins, VLDL - blood
Liver - drug effects - metabolism - pathology
Macrophages, Peritoneal - drug effects - metabolism
Male
Phagocytosis - drug effects
Prodigiozan - pharmacology
Rats
Rats, Wistar
Sterol O-Acyltransferase - metabolism
Stimulation, Chemical
Zymosan - pharmacology
Abstract
In this study we investigated the effects of zymosan and prodigiozan, the macrophage stimulators, and GdCl3, a macrophage inhibitor, on blood lipoprotein composition, activities of liver cholesterly ester (CE) metabolising enzymes, incorporation of [14C]cholesterol (C) into bile acids and accumulation and synthesis of CE in peritoneal macrophages (PM) of rats fed with C-enriched diet for 7 days. The increase of number of phagocyte cells quantity in liver and blood colony-stimulating activity in rats pretreated with intravenous injection of zymosan and prodigiozan was accompanied by reduced C content in blood low density and very low density lipoproteins (LDL and VLDL), increase of liver lysosomal CE hydrolase activity (without change of acyl-CoA:C acyltransferase and cytoplasmatic CE hydrolase activities) and incorporation of labeled C into bile acids and decrease of CE formation and accumulation in PM in rats with hypercholesterolemia. In contrast, reduction of phagocyte population in liver caused by intravenous injection of GdCl3 was accompanied by enhancement of C and CE level in blood LDL and VLDL and decrease of lysosomal CE hydrolase activity and incorporation of C into bile acids in liver of C-feeding rats. The data obtained suggest that the stimulation of mononuclear phagocyte system may lead to a decrease of plasma C via activation of LDL and VLDL catabolism and induction of bile acid synthesis in liver.
PubMed ID
12189625 View in PubMed
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Effects of Thermoextracts of Brucella S and L Forms on Lipid Peroxidation and Antioxidant Defense in Organs of Laboratory Animals.

https://arctichealth.org/en/permalink/ahliterature296008
Source
Bull Exp Biol Med. 2018 Jun; 165(2):239-242
Publication Type
Journal Article
Date
Jun-2018
Author
V I Dubrovina
S V Balakhonov
O V Yurieva
T P Starovoitova
N L Barannikova
L E Tokareva
A B Pyatidesyatnikova
K Yu Yastremskaya
T T Shkaruba
Author Affiliation
Irkutsk Antiplague Research Institute of Siberia and Far East, Irkutsk, Russia. dubrovina-valya@mail.ru.
Source
Bull Exp Biol Med. 2018 Jun; 165(2):239-242
Date
Jun-2018
Language
English
Publication Type
Journal Article
Keywords
Animal Structures - drug effects - metabolism
Animals
Animals, Laboratory
Antioxidants - metabolism
Brucella Vaccine - chemistry - pharmacology
Brucella abortus - chemistry - immunology - pathogenicity
Female
Guinea Pigs
L Forms - physiology
Lipid Peroxidation - drug effects
Liver - drug effects - metabolism - pathology
Male
Oxidative Stress - drug effects
Spheroplasts - physiology
Temperature
Vaccines, Attenuated - chemistry - pharmacology
Abstract
The dynamics of LPO marker malondialdehyde formation and peroxidase-destroying activity was studied in homogenized organs of guinea pigs, immunized with thermoextracts from S and L forms Brucella abortus I-206. The L form brucella thermoextract exhibited a lower reactogenicity and adequately activated the antioxidant system, due to which the destructive effects of ROS could be partially neutralized during the vaccinal process.
PubMed ID
29923000 View in PubMed
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FOXA transcription factors determine the amplitude of glucocorticoid induction of tyrosine aminotransferase in mice.

https://arctichealth.org/en/permalink/ahliterature92613
Source
Bull Exp Biol Med. 2007 Nov;144(5):722-4
Publication Type
Article
Date
Nov-2007
Author
Bryzgalov L O
Ershov N I
Ilnitskaya S I
Author Affiliation
Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences, Novosibirsk. leon_l@ngs.ru
Source
Bull Exp Biol Med. 2007 Nov;144(5):722-4
Date
Nov-2007
Language
English
Publication Type
Article
Keywords
Animals
Enzyme Activation - drug effects
Forkhead Transcription Factors - metabolism
Glucocorticoids - pharmacology
Liver - drug effects - metabolism - pathology
Liver Neoplasms - chemically induced - metabolism
Methyldimethylaminoazobenzene
Mice
Mice, Inbred ICR
Protein Binding - drug effects
Time Factors
Tyrosine Transaminase - metabolism
o-Aminoazotoluene
Abstract
o-Aminoazotoluene was more potent than 3'-methyl-4-dimethylaminoazobenzene in modulating glucocorticoid induction of tyrosine aminotransferase and DNA-binding activity of FOXA (HNF3) in 12-day-old ICR mice. In adult animals, induction of tyrosine aminotransferase and FOXA activity were modulated by o-aminoazotoluene, while 3'-methyl-4-dimethylaminoazobenzene was ineffective. Our results suggest that FOXA proteins determine glucocorticoid induction of tyrosine aminotransferase in mice (similarly to rats).
PubMed ID
18683506 View in PubMed
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[Hepatoprotective properties of liproxol]

https://arctichealth.org/en/permalink/ahliterature56631
Source
Eksp Klin Farmakol. 2002 Mar-Apr;65(2):31-3
Publication Type
Article
Author
A S Saratikov
Iu A Litvinenko
V N Burkova
A I Vengerovskii
V S Chuchalin
Author Affiliation
Pharmacology Department, Siberian Medical University, Moskovskii trakt 2, Tomsk, 634050 Russia.
Source
Eksp Klin Farmakol. 2002 Mar-Apr;65(2):31-3
Language
Russian
Publication Type
Article
Keywords
Animals
Antioxidants - therapeutic use
Carbon Tetrachloride Poisoning - drug therapy
Carotenoids - therapeutic use
Drug Combinations
English Abstract
Hepatitis, Toxic - drug therapy - mortality - pathology
Lipid Peroxidation - drug effects
Liver - drug effects - metabolism - pathology
Male
Metabolic Detoxication, Drug
Phospholipids - analysis - therapeutic use
Plant Extracts - therapeutic use
Rats
Abstract
The experiments on rats with a model toxic liver damage (tetrachloromethane hepatitis) showed evidence of a high hepatoprotector activity of liproxol, representing a combination of eplir and lokhein mixed in a 1-12 ratio. Liproxol inhibits lipid peroxidation, stimulates the excretory and detoxicant functions of liver, reduces hyperfermentation, and normalized membrane phospholipid composition.
PubMed ID
12109289 View in PubMed
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[Hepatotoxicity associated with the use of Herbalife]

https://arctichealth.org/en/permalink/ahliterature97845
Source
Laeknabladid. 2010 Mar;96(3):167-72
Publication Type
Article
Date
Mar-2010
Author
Magnús Jóhannsson
Sif Ormarsdóttir
Sigurdur Olafsson
Author Affiliation
magjoh@hi.is
Source
Laeknabladid. 2010 Mar;96(3):167-72
Date
Mar-2010
Language
Icelandic
Geographic Location
Iceland
Publication Type
Article
Keywords
Adult
Adverse Drug Reaction Reporting Systems
Aged
Alanine Transaminase - blood
Alkaline Phosphatase - blood
Bilirubin - blood
Biological Markers - blood
Biopsy
Cholestasis - chemically induced - diagnosis
Drug-Induced Liver Injury - diagnosis - etiology
Ephedra - adverse effects
Female
Humans
Iceland
Liver - drug effects - metabolism - pathology
Male
Middle Aged
Plant Preparations - adverse effects
Predictive value of tests
Risk assessment
Time Factors
Abstract
OBJECTIVE: Many herbal products are known to be hepatotoxic. In a recent survey in Iceland concerning adverse reactions related to herbal medicines, Herbalife products were implicated in the majority of the reported cases of hepatotoxicity. METHODS: The clinical presentations of five cases of Herbalife related liver injury during the period of 1999-2008 are analysed. Causality was assessed by using the WHO-UMC system for causality assessment and the RUCAM method. RESULTS: Of the five cases there were four females and one male; median age was 46 years (range 29-78). Herbalife had been used for 1 to 7 months prior to presentation. Four patients presented with a hepatocellular and one with a cholestatic reaction. Median values were for bilirubin 190 micromol/L (range: 26-311; ref.
PubMed ID
20197595 View in PubMed
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Liver resistance to CCl(4)-induced injury after stimulation of macrophages with various preparations.

https://arctichealth.org/en/permalink/ahliterature56663
Source
Bull Exp Biol Med. 2000 Jun;129(6):524-6
Publication Type
Article
Date
Jun-2000
Author
S N Kutina
A A Zubakhin
Author Affiliation
Research Center of Clinical and Experimental Medicine, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk.
Source
Bull Exp Biol Med. 2000 Jun;129(6):524-6
Date
Jun-2000
Language
English
Publication Type
Article
Keywords
Adjuvants, Immunologic - pharmacology
Alanine Transaminase - blood
Animals
Carbon Tetrachloride - toxicity
Hepatitis, Toxic - metabolism - pathology - prevention & control
Liver - drug effects - metabolism - pathology
Macrophages - drug effects - metabolism
Mannans - pharmacology
Muramidase - pharmacology
Peptidoglycan - pharmacology
Polysaccharides, Bacterial - pharmacology
Prodigiozan - pharmacology
Prostaglandins E - analysis
Rats
Rats, Wistar
Zymosan - pharmacology
Abstract
Acute toxic hepatitis in male Wistar rats was produced by single injection of 40% CCl(4) (0.2 ml per 100 g body weight in oil). Pretreatment with various immunostimulators (bacterial polysaccharides prodigiozan and salmozan; yeast polysaccharides zymosan, peptidoglycan, and mannan; and hydrolytic enzyme egg lysozyme) produced a hepatoprotective effect correlating which the stimulatory influence on macrophages and increasing in the following order: mannan
PubMed ID
11022238 View in PubMed
Less detail

P53 and Bcl2 apoptosis proteins in meso-2,3-dimercaptosuccinic acid treated lead-intoxicated rabbits.

https://arctichealth.org/en/permalink/ahliterature101912
Source
Toxicol Ind Health. 2011 Apr;27(3):271-8
Publication Type
Article
Date
Apr-2011
Author
Ehab Tousson
Bassem M Rafat
Mohamed Hessien
Ahmed A El Barbary
Ahmed Sami
Author Affiliation
Department of Zoology, Faculty of Science, Tanta University, Egypt. toussonehab@yahoo.com
Source
Toxicol Ind Health. 2011 Apr;27(3):271-8
Date
Apr-2011
Language
English
Publication Type
Article
Keywords
Animals
Bone and Bones - drug effects - metabolism - pathology
Brain - drug effects - metabolism - pathology
Chelating Agents - therapeutic use
Disease Models, Animal
Lead Poisoning - drug therapy - etiology - metabolism
Liver - drug effects - metabolism - pathology
Male
Organometallic Compounds - toxicity
Oxidation-Reduction
Oxidative Stress - drug effects
Oxyhemoglobins - metabolism
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rabbits
Succimer - therapeutic use
Tumor Suppressor Protein p53 - metabolism
Abstract
Lead (Pb) toxicity is one of the commonest environmental problems in our life; it causes many reversible and irreversible changes in our tissues. This study was carried out to investigate the effect of meso-2,3-dimercaptosuccinic acid (DMSA) on treatment of oxidative stress caused by lead poisoning in rabbits. Lead acetate (Pb(Ac)(2)) was orally administrated to rabbits for 21 days and then treated by DMSA for another 21 days. The effect of this treatment was investigated by measuring 2 of the apoptosis proteins p53 and Bcl2. Also, the auto-oxidation rate and their histopathological changes in brain, bone and liver were investigated. Hemoglobin auto-oxidation rate is measured as well as histopathological study of liver. Our data indicate that exposure to rabbits to Pb(Ac)(2) caused a significant increase of apoptosis protein p53 and decrease in the antiapoptotic BCl2 proteins.
PubMed ID
21112928 View in PubMed
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[The joint use of prednisolone and phospholipid-containing hepatoprotectors in experimental chronic hepatitis]

https://arctichealth.org/en/permalink/ahliterature56703
Source
Eksp Klin Farmakol. 1999 Mar-Apr;62(2):28-30
Publication Type
Article
Author
A I Vengerovskii
E L Golovina
M Iu Kovalenko
V S Chuchalin
E V Saprykina
N V Sosnina
V N Burkova
A S Saratikov
Author Affiliation
Department of Pharmacology, Siberian Medical University, Tomsk, Russia.
Source
Eksp Klin Farmakol. 1999 Mar-Apr;62(2):28-30
Language
Russian
Publication Type
Article
Keywords
Animals
Carbon Tetrachloride Poisoning - complications - drug therapy - metabolism - pathology
Carotenoids - therapeutic use
Drug Combinations
Drug Evaluation, Preclinical
Drug Therapy, Combination
English Abstract
Glucocorticoids - therapeutic use
Hepatitis, Chronic - drug therapy - etiology - metabolism - pathology
Hepatitis, Toxic - drug therapy - etiology - metabolism - pathology
Liver - drug effects - metabolism - pathology
Male
Phosphatidylcholines - therapeutic use
Phospholipids - therapeutic use
Prednisolone - therapeutic use
Rats
Abstract
In chronic CCl4-hepatitis in rats phospholipid-containing hepatoprotectors, essentiale and eplir differ in their influence on the therapeutic effect of prednisolone; essentiale does not change the antiproliferative effect of the glucocorticoid and weakens its membrane-stabilizing effect, eplir increases these therapeutic effects of prednisolone. Besides, eplir, in distinction from essentiale, reduces lipid accumulation in the liver and hypoproteinemia which are induced by prednisolone.
PubMed ID
10340125 View in PubMed
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[The pharmacological correction of the hepatotoxic action of platidiam]

https://arctichealth.org/en/permalink/ahliterature56707
Source
Eksp Klin Farmakol. 1999 Jan-Feb;62(1):62-4
Publication Type
Article
Author
T I Fomina
T V Vetoshkina
T Iu Dubskaia
Author Affiliation
Institute of Pharmacology, Tomsk Research Center, Siberian Branch, Russian Academy of Medical Sciences, Russia.
Source
Eksp Klin Farmakol. 1999 Jan-Feb;62(1):62-4
Language
Russian
Publication Type
Article
Keywords
Acute Disease
Animals
Antineoplastic Agents - toxicity
Carbon Tetrachloride Poisoning - drug therapy - metabolism - pathology
Cisplatin - toxicity
Cytophotometry
Drug Evaluation, Preclinical
English Abstract
Hepatitis, Toxic - drug therapy - etiology - metabolism - pathology
Histocytochemistry
Liver - drug effects - metabolism - pathology
Liver Regeneration - drug effects
Phosphatidylcholines - pharmacology - therapeutic use
Rats
Rats, Wistar
Time Factors
Abstract
A single intravenous infusion of 4.5 mg/kg of the new antineoplastic drug platidium induces structural-metabolic changes in the liver of rats (necrosis of hepatocytes, decrease of the glycogen and RNA content and accumulation of lipids in the cytoplasm of the hepatic cells, and increased activity of aspartate- and alaninaminotransferase in blood serum). An additional toxic factor (CCl4) applied one month after platidium infusion revealed incompleteness of reparative processes in the liver. The hepatoprotector essentiale weakens the injurious effect of the cytostatic on the hepatocytes and stimulates regeneration of the liver.
PubMed ID
10198772 View in PubMed
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10 records – page 1 of 1.