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)

The effect of ethanol on cells infected with mouse hepatitis virus (MHV) was investigated. After MHV infection of competent cells, NCTC1469, ethanol was added to the culture at various concentrations, and the viability of cells was measured using 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide. To examine the possible involvement of the ethanol metabolite, acetaldehyde, alcohol dehydrogenase activity was measured in NCTC1469 cells. Ethanol alone did not show cytotoxicity against NCTC1469 cells at concentrations from 0.125% to 2%. After infection with MHV, the viability of cells decreased, and this decrease was further enhanced, dose-dependently, by the addition of ethanol. The activity of alcohol dehydrogenase in the cells was below the detectable level. The same phenomena were also demonstrated in cells infected with influenza virus and Herpes simplex virus. These results demonstrate that ethanol enhances MHV-mediated cytotoxicity; this exacerbation of cytotoxicity by ethanol is suggested to be an effect common to cytopathic virus-infected cells.
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PMID:Effect of ethanol on mouse hepatitis virus-induced cytotoxicity. 888 34

The Hepatitis Delta Virus (HDV) ribozyme self-cleaving activity in 20 M formamide solutions is unique. Does this catalytic activity result from the conservation of its tertiary structure in 20 M formamide? We followed the ribozyme structure in formamide solutions by monitoring the amount of bound Ethidium Bromide (EB). We were able to measure the quantity of dye bound using time-resolved fluorescence spectroscopy, as an estimate of the ribozyme double helical content. This method, calibrated by using oligonucleotides with defined tertiary structure and denaturing solvents, parallels NMR and UV measurements as a function of temperature. Measurements with the HDV ribozyme lead to three conclusions: (a) both the precursor and product RNAs are structured to 24 M (95% w/w) formamide or 4 M H2O solutions which is equivalent to 4 M H2O; (b) the HDV ribozyme is the only RNA sequence investigated in this study that retains so much structure in formamide; and (c) DNA analogs of formamide resistant HDV ribozyme sequences lose their structure at less than 15 M formamide. Thus, the structural integrity of the HDV ribozyme is an intrinsic property of the RNA molecule and its sequence.
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PMID:Secondary structure content of the HDV ribozyme in 95% formamide. 891 91

Ethylene-di-bromide is a popular fumigant. Delayed long-term effects of this chemical include carcinogenicity and genotoxicity in animals. Only a few cases of acute ethylene-di-bromide toxicity have been reported and all of them have resulted in a fatal outcome. We report the first case of ethylene-di-bromide poisoning presenting with acute renal failure and toxic hepatitis that was managed successfully.
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PMID:Ethylene dibromide poisoning with acute renal failure: first reported case with non-fatal outcome. 1008 82

Acute quadriplegic myopathy is a rare condition associated with the use of nondepolarizing muscle-blocking agents and corticosteroids in the course of severe systemic illness. A 17-month-old boy underwent liver transplantation for fulminant hepatitis. He was intubated for 24 days and treated with vecuronium bromide and high-dose methylprednisolone. The child was weaned from the ventilator and presented extreme weakness in the upper limbs and total paralysis of the lower limbs. Serum creatine kinase level was normal and electromyography showed myopathic abnormalities. Muscle biopsy showed severe type-1 fiber atrophy and selective loss of myosin thick filaments was seen on electron microscopy. Scattered regenerating fetal myosin-positive fibers were present, mu calpain was absent, while m calpain was diffusely expressed. Physical therapy was immediately started and the child recovered even though corticosteroids were not discontinued. The pathogenesis of acute quadriplegic myopathy is still unknown. We suggest that it could be due to abnormal protein turnover in the muscle. Several independent factors, such as corticosteroid treatment, immobilization, or cytokines, could take part in a cascade of events that leads to an excessive yet selective degradation of proteins involving myosin thick filaments and possibly components of sarcolemma, causing muscle inexcitability.
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PMID:Acute quadriplegic myopathy in a 17-month-old boy. 1064 15

Hepatitis and fulminant hepatic failure have, infrequently, been associated with nimesulide. To establish if nimesulide or its analogues have direct cytotoxic activity on liver cells, experiments were undertaken to investigate the effects of nimesulide and its principal metabolites and production intermediates on the viability and growth of the human hepatoma cell line, HepG2, in vitro. The parent drug, metabolites or production intermediates as well as formulations of nimesulide were incubated for 6-48 hr with HepG2 cells and the extent of toxicity determined using the mitochondrial selective redox dye 3-4,5-dimethylthazol-2-yl)-2,4-diphenyl tetrazolium bromide (MTT). The results showed that there was no appreciable cytotoxic activity exhibited by nimesulide and its principle metabolites or production intermediates on HepG2 cells.
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PMID:Effects of nimesulide and its metabolites or manufacturing intermediates on the viability and growth of the human hepatoma HepG2 cell line. 1175 24

Some cyclic and acyclic nucleosides of thieno[2,3-d]-pyrimidine derivatives were synthesized via the reaction of compounds 1 and 2 or 3 and 4 with 2-chloroethyl methyl ether or 2,3,4, 6-tetra-O-acetyl-alpha-D-glucopyranosyl bromide. Nucleosides 9, 10, 15, and 16 were tested as antiviral agents against herpes simplex virus type-1 (HSV-1) and hepatitis-A virus (HAV). Compound 15 showed the highest effect on HSV-1 than the other three compounds, while the four tested compounds did not show any activity against HAV.
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PMID:Synthesis and antiviral screening of some thieno[2,3-d]pyrimidine nucleosides. 1644 Sep 82

Separation of atropisomers of analogues of the anti-hepatitis drug dimethyl diphenyl bicarboxylate (DDB) by capillary electrophoresis with vancomycin as the chiral selector is described. Among several tested chiral selectors, including various cyclodextrin derivatives as well as vancomycin, only the latter displayed the enantioselectivity to the studied atropisomers. However, relatively poor separation efficiency was obtained due to the adsorption of vancomycin on the capillary wall. This problem was overcome by modifying the capillary wall with a polycationic electrolyte named hexadimethrine bromide (HDB) to produce a positively charged coating, which minimized the adsorption of vancomycin on the capillary wall by electrostatic repulsion. Moreover, the positively charged coating could shorten the separation time by reversing the EOF because the reversed EOF migrated to the same direction as the negatively charged analyte. Effects of buffer pH, vancomycin and buffer concentrations and applied voltage on the separation were investigated and the optimal conditions were established as follows: 40 mM Tris-phosphate buffer (pH 6.0) containing 6.0 mM vancomycin and 0.001% HDB. Baseline separation of three racemic DDB analogues was obtained within 12 min under the optimal conditions.
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PMID:Separation of atropisomers of anti-hepatitis drug dimethyl diphenyl bicarboxylate analogues by capillary electrophoresis with vancomycin as the chiral selector. 1644 54

Most of the research on multiple sclerosis (MS) has focused on the early events that trigger demyelination and subsequent remyelination. Less attention has been given to the factors that directly mediate the demyelination that is the hallmark of the disease. Effector cells or molecules are those factors directly responsible for mediating the damage in the disease. Similarly, there are effector molecules that are critical for remyelination in the central nervous system (CNS). By understanding those effector molecules in demyelination and remyelination that directly influence the pathologic process, we should be able to generate specific therapies with the greatest potential for benefiting MS patients. This review focuses on effector cells and molecules that are critical for demyelination and remyelination in MS but also in experimental models of the disease including experimental autoimmune encephalomyelitis (EAE), virus-induced models of demyelination (Theiler's virus, murine hepatitis virus), and toxic models of demyelination (lysolecithin, ethidium bromide, and cuprizone). These are models in which the effector molecules for demyelination and remyelination have been most precisely evaluated.
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PMID:Effectors of demyelination and remyelination in the CNS: implications for multiple sclerosis. 1738 53

Bicyclol is a new generation of anti-hepatitis drug with China's own intellectual property rights. The chemical structure of bicyclol is new and original. Pharmacological research showed that it has high clinical efficacy in treating chronic hepatitis (HBV) patients and lower side effects. Two metabolites of bicyclol have been isolated: M2 (4-hydroxy-4'-methoxy-5, 6, 5', 6'-bis (methylenedioxy)-2-hydroxylmethyl-2'-methoxycarbonyl biphenyl) and M3 (4'-hydroxy-4-methoxy-5, 6, 5', 6'-bis (methyl enedioxy)-2-hydroxylmethyl-2'-methoxycarbonyl biphenyl). To further study the mechanism, safety, and effectiveness of bicyclol, the M2 and M3 have been total synthesized. The synthesis route is as following: the carboxyl and phenolic hydroxyl group of the aromatic bromide had been separately protected by bromobenzyl, coupling through the intermolecular asymmetric Ullmann reaction and then catalyst hydrogenated, borane reducted, two metabolites of bicyclol M2 and M3 were obtained. The structures were determined by IR, 1H NMR, HRMS. Comparison of hepatoprotective activity of bicyclol and the two metabolites on experimental liver injury, the potency of the metabolites were lower than that of bicyclol.
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PMID:[Synthesis of metabolites of bicyclol]. 1822 11

Osthole, 7-methoxy-8-[3-methylpent-2-enyl]coumarin (1), was extracted from a Chinese herb Cnidium monnieri (L.) Cuss. It showed immunity strengthening, anti-tumor, anti-hepatitis, and anti-osteoporosis activities in previous studies. Our goals are to study the effects of 1 on cell proliferation and TGF-beta of hypertrophic scar fibroblasts. Our results showed that 1 induced apoptosis and inhibited cell proliferation in hypertrophic scar fibroblasts. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that its IC(50) value toward hypertrophic scar fibroblasts was 15.5 +/- 2.2 micromol/l. Furthermore, the results of cell growth curve matched with the above results. Inducing apoptosis by 1 in hypertrophic scar fibroblasts was assessed by various morphological and biochemical characteristics, including cell shrinkage, chromatin condensation, membrane blebbing, formation of apoptotic bodies, and DNA ladder formation. A typical 'Sub-G(1) peak' was also checked through flow cytometry. We used immunohistochemistry to observe the expression of TGF-beta(1). Also, we found that 1 could obviously inhibit the expression of TGF-beta(1) of fibroblasts derived from hypertrophic scar compared with the control group (P < 0.05). These results suggest that 1 inhibits the growth of hypertrophic scar fibroblasts through apoptosis and decreases the expression of TGF-beta(1).
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PMID:Effects of osthole on apoptosis and TGF-beta1 of hypertrophic scar fibroblasts. 2018 4


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