• YAKHAK HOEJI
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• v.45 no.6
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• pp.641-649
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• 2001

In this study, the antitumor activities were investigated using $\beta$-lmmunan, a proteoglycan obtained from cultured mycelia of the IY009 strain of Ganoderma lucidum belonging to basidiomycetes. The result showed the significant effect of cytotoxicity test against murine sarcoma 180 and murine lymphocytic leukemia L1210 using immunized macrophage cultures by $\beta$-lmmunan. When intraperitoneally injected at 40 mg/kg/day daily for 10 days, $\beta$-lmmunan inhibited the growth of sarcoma 180 solid tumor in ICR mice by 88.8% (p<0.05). It was also observed that $\beta$-lmmunan increased life span by 85.2% (p<0.01) after treatment of 100 mg/kg/day in BDF1 mice bearing lymphocytic leukemia L1210. And combination therapy with cisplatin (dosage: 4 mg/kg) increased life span by 140.4% (p<0.05) after treatment of 100 mg/kg/day daily in BDF1 mice bearing lymphocytic leukemia L1210.

• Biomedical Science Letters
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• v.15 no.1
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• pp.67-72
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• 2009

Microtubule-interfering agents (MIAs), including paclitaxel, have been attributed in part to interference with microtubule assembly, impairment of mitosis, and changes in cytoskeleton. But the signaling mechanisms that link microtubule disarray to destructive or protective cellular responses are poorly understood. This study investigated the effect of paclitaxel on differentiation such as type II collagen expression and sulfated proteoglycan accumulation in rabbit articular chondrocytes. Paclitaxel caused differentiated chondrocyte phenotype as demonstrated by increment of type II collagen expression and proteoglycan synthesis Paclitaxel treatment stimulated activation of ERK-1/2 and p38 kinase. Inhibition of ERK-1/2 with PD98059 enhanced paclitaxel-induced differentiation, whereas inhibition of p38 kinase with SB203580 suppressed paclitaxel-induced differentiation. Our findings suggest that ERK-1/2 and p38 kinase oppositely regulate paclitaxel-induced differentiation in chondrocytes.

• YAKHAK HOEJI
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• v.43 no.5
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• pp.635-641
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• 1999

In this study, we investigated the immunopotent activities of lepidan, a water soluble proteoglycan from Lentinus lepideus. To examine whether lepidan may affect nonspecific immune responses, we determined the effect on the production of nitric oxide (NO). Lepidan effectively increased the NO production in IFN-${\gamma}$ and LPS triggered RAW 264.7 cells. To further demonstrate the evidence that lepidan activates various immune cells, we determined the alkaline phosphatase activity, plaque-forming cell number and secretion of interleukine-4 (IL-4) and granulocyte/macrophage-colony stimulating factor (GM-CSF) after lepidan treatment in murine splenocytes. The results showed that lepidan increased alkaline phosphatase activity and the number of plaque-forming cells, which indicates that lepidan can lead B lymphocytes to late stage of differentiation. Also, when the splenocytes were cultured with lepidan for 48 hr, the level of IL-4 and GM-CSF in the supernatant dramatically increased. Taken together, these data suggest that lepidan is a biological response modulator that is able to activate immune responses.

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.859-859
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• 2005

• The Journal of the Korean Society for Microbiology
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• v.34 no.5
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• pp.435-443
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• 1999

Orientia tsutsugamushi is obligate intracellular bacterium that grows within the cytoplasm of the eukaryotic host cells. Therefore capability of the attachment, entry into the host cell and intracellular survival should be critical process for oriential infection. In this study we investigated the cellular invasion mechanism of Orientia tsutsugamushi and the role of transmembrane heparan sulfate proteoglycan, which binds diverse components at the cellular microenvironment and is implicated as host cell receptors for a variety of microbial pathogens. First of all Orientia tsutsugamushi can invade a wide range of nonprofessional phagocytic cells including fibroblast, epithelial cells and endothelial cells of various host species, including Band T lymphocytes. Thus, it was postulated that the attachment of O. tsutsugamushi requires the recognition of ubiquitous surface structures of many kinds of host cells. Treatments with heparan sulfate and heparin inhibited the infection of Orientia tsutsugamushi in dose-dependent manner for L cell, mouse fibroblast, whereas other glycosaminoglycans such as chondroitin sulfate had no effect. Collectively, these findings provide strong evidence that initial interaction with heparan sulfate proteoglycan is required for the oriential invasion into host cells.

• The Journal of Korean Medicine
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• v.27 no.1 s.65
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• pp.229-239
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• 2006

Objectives : Articular cartilage is a potential target for drugs designed to inhibit the activity of matrix metalloproteinases (MMPs) to stop or slow the destruction of the proteoglycan and collagen in the cartilage extracelluar matrix. The purpose of this study was to investigate the effects of KHBJs for cartilage-protective effect in human and rabbit articular cartilage explants. Methods : The cartilage-protective effects of KHBJ were evaluated by using glycosaminoglycan degradation assay, collagen degradation assay, colorimetric analysis of MMPs activity, and histological analysis in rabbit and human cartilage explants culture. Results : KHBJs significantly inhibited GAG and collagen release of rabbit and human cartilage explant in a concentration-dependent manner. Also, KHBJs inhibited MMP-3 and MMP-13 activities from IL-$1{\alpha}$-treated cartilage explants cultures. Histological analysis indicated that KHBJ004 reduced the degradation of the cartilage matrix compared with that of IL-$1{\alpha}$-treated cartilage explants. KHBJ004 had no harmful effect on chondrocytes viability or cartilage morphology in cartilage explants. Conclusions : These results indicate that KHBJs inhibits the degradation of proteoglycan and collagen through the downregulation of MMP-3 and MMP-13 activities without affecting the viability or morphology of IL-$1{\alpha}$-stimulated rabbit and human articular cartilage explants.

• Biomolecules & Therapeutics
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• v.21 no.6
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• pp.447-453
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• 2013

Chondroitin sulfate proteoglycan (CSPG) inhibits neurite outgrowth of various neuronal cell types, and CSPG-associated inhibition of neurite outgrowth is mediated by the Rho/ROCK pathway. Mesenchymal stromal/stem cells (MSCs) have the potential to differentiate into neuron-like cells under specific conditions and have been shown to differentiate into neuron-like cells by co-treatment with the ROCK inhibitor Y27632 and the hypoxia condition mimicking agent $CoCl_2$. In this study, we addressed the hypothesis that a ROCK inhibitor might be beneficial to regenerate neurons during stem cell therapy by preventing transplanted MSCs from inhibition by CSPG in damaged tissues. Indeed, dose-dependent inhibition by CSPG pretreatment was observed during morphological changes of Wharton's jelly-derived MSCs (WJ-MSCs) induced by Y27632 alone. The formation of neurite-like structures was significantly inhibited when WJ-MSCs were pre-treated with CSPG before induction under Y27632 plus $CoCl_2$ conditions, and pretreatment with a protein kinase C inhibitor reversed such inhibition. However, CSPG treatment resulted in no significant inhibition of the WJ-MSC morphological changes into neuron-like cells after initiating induction by Y27632 plus $CoCl_2$. No marked changes were detected in expression levels of neuronal markers induced by Y27632 plus $CoCl_2$ upon CSPG treatment. CSPG also blocked the morphological changes of human bone marrow-derived MSCs into neuron-like cells under other neuronal induction condition without the ROCK inhibitor, and Y27632 pre-treatment blocked the inhibitory effect of CSPG. These results suggest that a ROCK inhibitor can be efficiently used in stem cell therapy for neuronal induction by avoiding hindrance from CSPG.

• Microbiology and Biotechnology Letters
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• v.41 no.3
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• pp.379-382
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• 2013

In order to investigate the anticancer activity of an anti-yeast substance (AYS), a proteoglycan produced by Rhanella aquatilis AY2000, the cytotoxicity of the AYS against cancer cells was determined in vitro. The AYS was not cytotoxic to the human Jurkat T cell or the mouse sarcoma 180 cell, but was cytotoxic to the human colon cancer TH20 cell. The AYS was increasingly cytotoxic against human colon cancer cells in a dose-dependent manner at range from 62.5 to 500 ${\mu}g/ml$. Anticancer activity by combination of the AYS and an anticancer agent was also determined. The anticancer agent combined with the AYS was shown to possess greater synergistic anticancer activity against human colon cancer cells, as compared with the anticancer agent alone.

• Analytical Science and Technology
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• v.28 no.1
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• pp.72-77
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• 2015

To study the efficacy of extract powder of Angelica gigas in preventing and treating degeneration of the articular cartilage in rats with monosodium iodoacetate (MIA)-induced osteoarthritis, A total of 30 six-week-old Sprague-Dawley rats were randomly divided into normal control group, untreated group and Angelica gigas treated group, with 10 rats in each group. During the treatment period, body weight were measured in each four days interval from starting date. The rat were sacrificed at the end of 3rd week after daily administration of Angelica gigas and then rat tibia articular cartilage was removed. In articular cartilages, glycosaminoglycan (GAG) amount increased by MIA treatment were reduced while proteoglycan (PG) amount decreased by MIA treatment were fairly recovered by Angelica gigas treatment, respectively. The content of TNF-a was also slightly reduced sections of the cartilage were stained with safranin-0 were also partially recovered by Angelica gigas treatment. By HPLC analysis, the content of main compounds decursin and decursinol angelate was analyzed as $10.5{\pm}0.2%$ of total extracts.

• Journal of Korean Medicine Rehabilitation
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• v.27 no.2
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• pp.9-17
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• 2017

Objectives This study was aimed to evaluate the effects of Daeyoungjeon (hereinafter referred to DYJ) treatment on the injury of articular cartilage induced by monosodium iodoacetate in rats. Methods Twenty-four male rats were divided into normal, osteoarthritic control and DYJ group. Rats of normal group were injected with 0.1 ml physiological saline, rats of control and DYJ groups were injected with 0.1 ml monosodium iodoacetate (3 mg/ml) into each left and right knee joint cavities. Rats of DYJ group were administrated extracts of DYJ during 60 days per orally. At 60 days after treatment, gross lesions, area and proteoglycan contents of articular cartilage, histopathological lesions, immunohistochemistry on matrix metalloproteinases (MMP-2, MMP-3, MMP-7) were evaluated. Results Grossly, degenerative changes of articular cartilages were observed weak in DYJ group. The areas of articular cartilages were broader significantly in DYJ group. The proteoglycan contents in articular cartilages were lesser significantly in DYJ group. Histopathologically, the chondrocyte score was lesser significantly in DYJ group. MMP-3 expression in articular cartilages was observed weak in DYJ group. Conclusions From above results, DYJ treatment has inhibitory effects on the injuries of articular cartilage induced by monosodium iodoacetate in rats, and it's effects may be related with down regulation of MMP-3.