OBJECTIVETo further study the mechanism of the inhibitory effect of interferon beta-1a (IFN beta-1a) on the activation of human hepatic stellate cell (HSC) LX-2, and to analyze the differences on the protein expression in LX-2 induced by I IFN beta-1a.

METHODSCultured LX-2 cells were treated with 2000 U/ml IFN beta-1a for 48 h. Two-dimensional gel electrophoresis (2-DE) was performed to compare protein patterns of the control (untreated) and IFN beta-1a treated LX-2 and for quantitative and qualitative analyses of protein expression. A rat liver fibrosis model was established and the rats were sacrificed and their various tissues were obtained for the same analyses. Western blotting and RT-PCR were used to validate the expression of the changed proteins after treatment of IFN beta-1a in LX-2 cells and of various tissues of the rats.

RESULTS708 +/- 25 spots were detected in control LX-2 cells and 804 +/- 32 spots in IFN beta-1a-treated LX-2 cells. A match rate of 73%-82% was achieved. The results also showed that 31 protein spots displayed quantitative changes in expression after IFN beta-1a treatment. Of the 31 spots, 21 proteins were identified, of which, one was newly found, two were enhanced in abundance and 18 showed lower expressions. The newly found protein was glia maturation factor beta (GMF beta). The treatment of LX-2 with IFN beta-1a increased the production of GMF beta(GMF beta) protein in comparison with the untreated cells (t=1.81, P < 0.01). The expression of GMF beta protein (1.81 vs 0.10) and mRNA (0.85 vs 0.12) were more in the normal liver tissues than in the cirrhotic liver tissues (t=2.53, 2.13 respectively, P < 0.01). The expressions of GMF beta protein and mRNA were weak in rat heart and lung tissues, however, they were strong in rat liver, kidney, spleen and brain tissues (t=1.91, 1.94 respectively, P < 0.01).

CONCLUSIONThere is a significant difference of protein expression levels between IFN beta-1a untreated and treated LX-2 cells. These proteins, especially GMF beta, may be involved in an inhibition process of IFN beta-1a on activation and apoptosis of LX-2 cells. This proteome study may be useful in further studies of the relationship of IFN beta-1a treatment and human liver diseases.

Animals ; Cell Line ; Female ; Glia Maturation Factor ; metabolism ; Hepatic Stellate Cells ; metabolism ; Humans ; Interferon beta-1a ; Interferon-beta ; pharmacology ; Liver ; cytology ; Liver Cirrhosis ; metabolism ; Proteome ; Rats ; Rats, Sprague-Dawley

STUDY DESIGN: Level 1 randomized controlled study. PURPOSE: To investigate the effects of systemic and local interferon-beta-1a (IFN-β-1a) on prevention of epidural fibrosis using histopathological parameters. OVERVIEW OF LITERATURE: Epidural fibrosis involves fibroblastic invasion of nerve roots into the epidural space. Formation of dense fibrous tissue causes lumbar and radicular pain. Many surgical techniques and several materials have been proposed in the literature, but no study has assessed the effect of IFN-β-1a on prevention of epidural fibrosis. METHODS: Forty-eight adult female Sprague-Dawley rats were divided into six groups of eight: sham group, control group, systemic 44 μg IFN-β-1a group and 22 μg IFN-β-1a group (after laminectomy and discectomy, 0.28 mL and 0.14 mL IFN-β-1a applied subcutaneously three times for a week, respectively), local 44 μg IFN-β-1a group (laminectomy and discectomy, followed by 0.28 mL IFN-β-1a on the surgical area), and local 22 μg IFN-β-1a group (laminectomy and discectomy, followed by 0.14 mL IFN-β-1a on the surgical area). All rats were sacrificed after 4 weeks and groups were evaluated histopathologically. RESULTS: Compared with sham and control groups, significantly less epidural fibrosis, dural adhesion, and fibroblast cell density were observed in the local and systemic 44 μg IFN-β-1a groups. No other differences were evident between the local and systemic groups. CONCLUSIONS: IFN-β-1a is effective in preventing epidural fibrosis with systemic and local application.
Adult ; Animals ; Cell Count ; Control Groups ; Diskectomy ; Epidural Space ; Female ; Fibroblasts ; Fibrosis* ; Humans ; Interferon beta-1a* ; Interferons* ; Laminectomy ; Rats ; Rats, Sprague-Dawley

STUDY DESIGN: Level 1 randomized controlled study. PURPOSE: To investigate the effects of systemic and local interferon-beta-1a (IFN-β-1a) on prevention of epidural fibrosis using histopathological parameters. OVERVIEW OF LITERATURE: Epidural fibrosis involves fibroblastic invasion of nerve roots into the epidural space. Formation of dense fibrous tissue causes lumbar and radicular pain. Many surgical techniques and several materials have been proposed in the literature, but no study has assessed the effect of IFN-β-1a on prevention of epidural fibrosis. METHODS: Forty-eight adult female Sprague-Dawley rats were divided into six groups of eight: sham group, control group, systemic 44 μg IFN-β-1a group and 22 μg IFN-β-1a group (after laminectomy and discectomy, 0.28 mL and 0.14 mL IFN-β-1a applied subcutaneously three times for a week, respectively), local 44 μg IFN-β-1a group (laminectomy and discectomy, followed by 0.28 mL IFN-β-1a on the surgical area), and local 22 μg IFN-β-1a group (laminectomy and discectomy, followed by 0.14 mL IFN-β-1a on the surgical area). All rats were sacrificed after 4 weeks and groups were evaluated histopathologically. RESULTS: Compared with sham and control groups, significantly less epidural fibrosis, dural adhesion, and fibroblast cell density were observed in the local and systemic 44 μg IFN-β-1a groups. No other differences were evident between the local and systemic groups. CONCLUSIONS: IFN-β-1a is effective in preventing epidural fibrosis with systemic and local application.
Adult ; Animals ; Cell Count ; Control Groups ; Diskectomy ; Epidural Space ; Female ; Fibroblasts ; Fibrosis* ; Humans ; Interferon beta-1a* ; Interferons* ; Laminectomy ; Rats ; Rats, Sprague-Dawley

Multiple sclerosis (MS) is a demyelinating disorder that affects discrete areas of the CNS, including the optic nerves, in a quite variable relapsing-remitting fashion over a prolonged period of time. Although MS is usually considered to be a disease that affects peoples in early to middle adulthood, children do develop multiple sclerosis. The frequency of MS onset before the age of 15 years is 2.7-5% of all cases, while MS onset during infancy and early childhood was observed to be 0.2- 0.7% of all cases. We report here on a Korean case of a relapsing-remitting MS female child who was treated with four rounds of intravenous methylpredinsolone pulse therapy and preventive Interferon-beta-1b (Betaferon(R)).
Child ; Demyelinating Diseases ; Female ; Humans ; Interferons* ; Multiple Sclerosis* ; Optic Nerve ; Interferon beta-1b

Here we report a case of pediatric multiple sclerosis treated with interferon beta-1b. Interferon beta is widely used in adult patients with multiple sclerosis (MS). However, its effects and safety in pediatric patients have not been well established. Although supporting data are limited, the use of disease modifying therapies (DMTs) such as interferon beta-1b is recommended early in treatment of children with MS. Reports of interferon beta treatment in pediatric MS patients in Korea are rare. In this report, we describe a Korean girl who was effectively treated with interferon beta-1b for three years. There were no relapses or serious side effects. Therefore, this report provides evidence supporting the use of interferon beta in pediatric MS patients in Korea and other Asian countries. We also reviewed current medical treatment of MS, including some DMTs and second-line treatment options such as natalizumab and cyclophosphamide, and several new oral agents such as fingolimod.
Adult ; Antibodies, Monoclonal, Humanized ; Asian Continental Ancestry Group ; Child ; Cyclophosphamide ; Humans ; Interferon-beta ; Interferons ; Korea ; Multiple Sclerosis ; Propylene Glycols ; Recurrence ; Sphingosine ; Fingolimod Hydrochloride ; Interferon beta-1b ; Natalizumab

No abstract available.
Humans ; Interferon-beta* ; Interferons* ; Multiple Sclerosis ; Multiple Sclerosis, Relapsing-Remitting*

No abstract available.
Humans ; Interferon-beta* ; Interferons* ; Multiple Sclerosis ; Multiple Sclerosis, Relapsing-Remitting*

No abstract available.
Humans ; Interferon-beta ; Interferons ; Multiple Sclerosis ; Porphyria Cutanea Tarda ; Porphyrias

The study was aimed to investigate the synergistically effect of interferon-α (IFN-α) and homoharringtonine (HHT) on the proliferation, apoptosis, cell cycle of K562 cells and the expression of &beta;-catenin. The proliferation, apoptosis, cell cycle and &beta;-catenin mRNA expression of K562 cells treated with IFN-α and/or HHT were assayed with MTT, flow cytometry or RT-PCR respectively. The results showed that HHT alone, but not IFN-α alone, displayed a proliferation inhibition, apoptosis induction, G(0)/G(1) phase block and down-regulation of &beta;-catenin expression in K562 cells with concentration- and time-dependent manners. The expression level of &beta;-catenin mRNA after being treated with HHT was 0.5576 ± 0.0373, which were lower than that in control group (0.9369 ± 0.0142). The down-regulation of &beta;-catenin expression in group of IFN-α combined with HHT was higher significantly than that in HHT group (0.3737 ± 0.0529 vs 0.5576 ± 0.0373, P < 0.05). Otherwise, HHT combined with IFN-α did not demonstrate obvious toxicologic effect on bone marrow mononuclear cells. It is concluded that IFN-α combined with HHT can enhance the cytotoxic effect of HHT on K562 cells, which may be associated with down-regulation of &beta;-catenin expression.
Cell Proliferation ; drug effects ; Harringtonines ; pharmacology ; Humans ; Interferon-alpha ; pharmacology ; K562 Cells ; beta Catenin ; genetics ; metabolism

Cell Line ; Hepatic Stellate Cells ; drug effects ; metabolism ; Humans ; Interferon-beta ; pharmacology