Hye-Jin Park

Sungkyunkwan University, Seoul, Seoul, South Korea

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Publications (10)23.27 Total impact

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    ABSTRACT: Bone cell proliferation, bone formation, and bone resorption are the main factors involved in the homeostasis of the bone mass. Osteoblast death is a problem experienced by postmenopause women. Herbal medicines have attracted considerable attention for use as a drug or a drug substitute in the treatment of bone-related diseases, such as osteoporosis. This study investigated the effects of kobophenol A on the proliferation in human osteoblast cells. Kobophenol A stimulated the proliferation of osteoblast cells by the increases in DNA synthesis and the enhancement of cell cycle progression. Kobophenol A stimulation induced the expression of the cyclin B1 and cyclin-dependent kinase 1 (CDK1). Treatment of osteoblast cells with p38 MAPK inhibitor SB203580 significantly inhibited kobophenol A-enhanced proliferation. In addition, kobophenol A induced phosphorylation of p38 MAPK. Treatment of osteoblast cells with kobophenol A resulted in improvement of ROS scavenging activity. Moreover, kobophenol A treatment up-regulated the Bcl-2 level, but down-regulated the level of Bax expression. We also demonstrate that kobophenol A increased alkaline phosphatase (ALP) activity after 2days. Taken together, the results of this study reveal that kobophenol A has proliferative effects and enhances ALP activity in osteoblast cells and these findings provide insights into the development of a therapeutic approach of kobophenol A in the prevention of osteoporosis and other bone disorders.
    International immunopharmacology 09/2013; · 2.21 Impact Factor
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    ABSTRACT: Atherosclerosis is a chronic inflammatory disease associated with increased expression of adhesion molecules in vascular smooth muscle cells (VSMCs). The objective of this study was to examine the in vitro effects of extract from aerial Bulbil of Dioscorea batatas Decne (Db-Ex) on the ability to suppress the expression of adhesion molecules induced by TNF-α. We also identified bioactive components from a methanol extract. VSMCs pre-exposed to Db-Ex (10-100 μg/ml) were stimulated with TNF-α (10 ng/ml). Preincubation of VSMCs for 2 h with Db-Ex dose-dependently inhibited TNF-α-induced adhesion of THP-1 monocytic cells and mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Db-Ex treatment decreased ROS production and the amount of phosphorylated form of p38, ERK, JNK and Akt in TNF-α-stimulated cells, suggesting that Db-Ex inhibits adhesion molecule expression possibly through MAPK and Akt regulation. Db-Ex also suppressed TNF-α-activation NK-κB. This effect was mediated through degradation of IκBα and nuclear translocation of the p65 subunit of NF-κB. These results suggest that Db-Ex inhibits monocyte adhesion and the TNF-α-mediated induction of adhesion molecules in VSMC by downregulating the MAPK/Akt/NF-κB signaling pathway, which may explain the ability of Db-Ex to suppress inflammation within the atherosclerotic lesion.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 05/2012; 50(8):2792-804. · 2.99 Impact Factor
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    ABSTRACT: Atherosclerosis is a long-term inflammatory disease of the arterial wall. Increased expression of the cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) is associated with increased proliferation of vascular smooth muscle cells (VSMCs), leading to increased neointima or atherosclerotic lesion formation. Therefore, the functional inhibition of adhesion molecules could be a critical therapeutic target of inflammatory disease. In the present study, we investigate the effect of sulforaphane on the expression of VCAM-1 induced by TNF-α in cultured mouse vascular smooth muscle cell lines. Pretreatment of VSMCs for 2h with sulforaphane (1-5μg/ml) dose-dependently inhibited TNF-α-induced adhesion of THP-1 monocytic cells and protein expression of VCAM-1. Sulforaphane also suppressed TNF-α-induced production of intracellular reactive oxygen species (ROS) and activation of p38, ERK and JNK. Furthermore, sulforaphane inhibited NK-κB and AP-1 activation induced by TNF-α. Sulforaphane inhibited TNF-α-induced ΙκΒ kinase activation, subsequent degradation of ΙκΒα and nuclear translocation of p65 NF-κB and decreased c-Jun and c-Fos protein level. This study suggests that sulforaphane inhibits the adhesive capacity of VSMC and downregulates the TNF-α-mediated induction of VCAM-1 in VSMC by inhibiting the MAPK, NF-κB and AP-1 signaling pathways and intracellular ROS production. Thus, sulforaphane may have beneficial effects to suppress inflammation within the atherosclerotic lesion.
    Vascular Pharmacology 12/2011; 56(3-4):131-41. · 3.21 Impact Factor
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    ABSTRACT: Atopic dermatitis (AD) is an allergic, inflammatory skin disease characterized by chronic eczema and mechanical injury to the skin, caused by scratching. Korean red ginseng (RG) has diverse biological activities, but the molecular effects of RG on allergic diseases, like AD, are unclear. The present study was designed to investigate whether RG inhibits 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD in a mouse model. DNCB was applied topically on the dorsal surface of Balb/c mice to induce AD-like skin lesions. We observed the scratching behavior and examined the serum IgE level and interleukin (IL)-4 and IL-10 in splenocytes compared with dexamethasone. We also evaluated the DNCB-induced mitogen-activated protein kinases (MAPKs), NF-κB, and Ikaros activities after RG treatment using reverse transcriptase-polymerase chain reaction, Western blotting, and ELISA. Our data showed that the topical application of RG significantly improved the AD-like skin lesions and scratching behavior. RG decreased not only the mRNA expression of IL-4 and IL-10, but also the secretion of IL-4 protein and serum IgE in mice. Additionally, RG treatment decreased the DNCB-induced MAPKs activity and subsequent Ikaros translocation irrespective of NF-κB. We suggest that RG may be useful as a therapeutic nutrition for the treatment of AD.
    Journal of ginseng research 11/2011; 35(4):479-486. · 2.26 Impact Factor
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    ABSTRACT: Acrylamide has been known to have a neurotoxic effect which is associated with nerve damage in both the central and peripheral nervous systems. Since neural cell adhesion molecule (NCAM) plays an important role in the processes of neuronal development and synaptic plasticity, the down-regulation of NCAM may lead impaired spatial memory and reduced long-term potentiation. We examined the effect of acrylamide on NCAM expression and the mechanisms of its effect in human neuroblastoma cells. Treatment with acrylamide resulted in the decrease of NCAM expression, which was reversed by CK2 inhibitor, 4,5,6,7-tetrabromobenzotriazole (TBB). Moreover, Western blot analysis showed that acrylamide induced the expression of CK2. Acrylamide dose-dependently decreased the DNA binding affinity of the Ikaros transcription factor, which is a bifunctional differentiation factor. In addition, the cells treated with acrylamide and CK2 inhibitor showed increased Ikaros activity compared with the acrylamide treatment only. Small interfering RNA-mediated depletion of CK2-α also increased Ikaros activity in acrylamide-treated cells. Overall, these data suggest that acrylamide decreases the Ikaros DNA binding activity via the CK2 pathway, resulting in a decrease of NCAM expression and provide further insight into the mechanisms underlying acrylamide actions.
    Toxicology in Vitro 10/2010; 24(7):1946-52. · 2.65 Impact Factor
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    ABSTRACT: Atherosclerosis is a chronic inflammatory disease and the expression of adhesion molecules on vascular smooth muscle cells (VSMCs) contributes to the progress of the disease. Diosgenin, a precursor of steroid hormones, has been shown to have a variety of biological activities including anti-inflammatory activity; however, its molecular mechanisms are poorly understood. This study examined the effect of diosgenin on the expression of adhesion molecules induced by TNF-α in cultured mouse VSMC cell line, MOVAS-1. Preincubation of VSMCs for 2h with diosgenin (0.1-10 μM) dose-dependently inhibited TNF-α-induced adhesion of THP-1 monocytic cells and mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Diosgenin abrogated TNF-α induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38, ERK, JNK and Akt. Diosgenin was also shown to inhibit NK-κB activation induced by TNF-α. Furthermore, diosgenin inhibited TNF-α-induced IκB kinase activation, subsequent degradation of IκBα, and nuclear translocation of NF-κB. Our results indicate that diosgenin inhibits the adhesive capacity of VSMC and the TNF-α-mediated induction of ICAM-1 and VCAM-1 in VSMC by inhibiting the MAPK/Akt/NF-κB signaling pathway and ROS production, which may explain the ability of diosgenin to suppress inflammation within the atherosclerotic lesion and modulate immune response.
    Vascular Pharmacology 10/2010; 53(5-6):273-80. · 3.21 Impact Factor
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    ABSTRACT: Diosgenin is a precursor of steroid hormones, which can be found in several plant species. Diosgenin has been shown to have a variety of biological activities including anti-inflammatory activity, but through a mechanism that is unclear. Especially, the effect of this agent on macrophage function has not been characterized in detail. In the present study, we examined the effects of diosgenin on the production of inflammatory mediators in lipopolysaccharide (LPS)/interferon gamma (IFN-gamma)-activated murine macrophage. Macrophages pre-exposed to diosgenin (0.1-10 microM) were stimulated with LPS/IFN-gamma. Pretreatment with diosgenin resulted in the inhibition of NO production and inducible nitric oxide synthase (iNOS) protein and mRNA expression in a concentration-dependent manner. In addition, diosgenin inhibits production of reactive oxygen species (ROS), interleukin-1 (IL-1), and IL-6, but not that of tumor necrosis factor-alpha (TNF-alpha). Inhibition of these inflammatory mediators appears to be at the transcriptional level, since diosgenin decreased LPS/IFN-gamma-induced NF-kappaB and AP-1 activity. Diosgenin blocked CK2 activation and phosphorylation of c-Jun NH(2)-terminal kinase (JNK), but not that of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 (ERK 1/2). These results indicate that the inhibition of these signaling molecules expression was correlated with the reduced production of inflammatory mediators in macrophages. Taken together the present data suggest that diosgenin reduces the production of inflammatory meditators by inhibiting LPS/IFN-gamma-triggered CK2, JNK, NF-kappaB and AP-1 activation, thereby implicating a mechanism by which diosgenin may exert its immunosuppressive effects.
    International immunopharmacology 09/2010; 10(9):1047-54. · 2.21 Impact Factor
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    ABSTRACT: Rosa rugosa has been used as a folk medicine with various pharmacological properties for a long time in Asia. We investigated effects of fructus extracts of Rosa rugosa (RRF) and semen extracts of this herb (RRS) on bone forming cells (osteoblastic and pre-osteoclastic cells) to evaluate the pharmacological possibilities in a variety of bone-related disease. RRF showed significant effect on proliferation of osteoblastic cells in dose-dependent manners at 72 hrs and of RRS was effective at 48 and 72 hrs. RRF and RRS did not decreased production of TNF- but NO by pre-osteoclastic cells under inflammation circumstance indeced by LPS. We also investigated the effects of RRF and RRS on the mitogen-induced lymphocyte proliferation in the old and young mice in ex vivo systems. RRF and RRS significantly enhanced proliferative effects of untreated and ConA-treated splenocytes from the old and young mice. But, RRS at increased LPS-induced TNF- production in pre-osteoclastic cells and reduced LPS-stimulated lymphoblastogenesis in the old and young at . These results indicate that RRF has beneficial effects on osteoarthritis and give further possibilities for the immunomodulating effects not only in old that has more frequent bone related diseases but also in young.
    Korean Journal of Plant Resources. 01/2010; 23(2).
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    ABSTRACT: Allergies are immediate hypersensitive responses to antigens and interleukin (IL)-4 is involved in the initiation and development of allergic responses. has been known to have a variety of biological activities including anti-inflammatory activity, but the effect of on allergic responses is not known yet. The present study was undertaken to examine whether has an inhibitory effect on allergic response in mouse model. In allergic mouse model, our results showed that topical application of on atopic dermatitis (AD)-like skin lesions improved skin condition and inhibited starching behaviors. In addition, application not only suppressed mRNA expression of IL-4 and IL-10, but also prevented the nuclear factor of activated T cells 1 transcription. Moreover, application suppressed IL-4's secretion. Taken together, these results suggest that has a potent inhibitory effect in AD-related T cell cytokine production and may be a candidate for therapeutic agent in allergy.
    Journal of ginseng research 01/2010; 34(4). · 2.26 Impact Factor
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    ABSTRACT: Macrophages play an important role in the first line of immunologic effects against tumor cells. The effects of nonsaponin red ginseng (NSRG) components on macrophage functions like tumoricidal activity, phagocytic activity, and NO production in young (8-weeks-old) and aged (82-weeks-old) male C57BL/6 mice were assessed in vitro, respectively. The treatment of tumor cells (melanoma B16 cells) with the supernatants of NSRG-treated macrophages resulted in an increase of cytotoxicity at 300 g/ml in the aged mice, whereas the supernatants did not have a cytotoxic effect in the young mice. It was observed that the supernatants induced the increase of tumor cell proliferation at 150 g/ml in the young mice, suggesting that the supernatants contain growth factors rather than cytotoxic molecules. In addition, NSRG alone had a direct cytotoxic effect on the B16 tumor cells. NSRG had no effect on the NO production by the macrophages in the young mice, while it significantly increased the level of NO release in the aged mice. There was no difference in the phagocytic activities of the macrophages by NSRG in both groups of mice. These results suggest that NSRG has differential effects on the macrophage functions in young and aged mice.
    Journal of ginseng research 01/2009; 33(3). · 2.26 Impact Factor