Eun Mi Choi

Kyung Hee University, Sŏul, Seoul, South Korea

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Publications (72)160.55 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Methylglyoxal (MG), a highly reactive metabolite of hyperglycemia, can enhance protein glycation, oxidative stress or inflammation. The present study investigated the effects of apocynin on the mechanisms associated with MG toxicity in osteoblastic MC3T3-E1 cells. Pretreatment of MC3T3-E1 cells with apocynin prevented the MG-induced protein glycation and formation of intracellular reactive oxygen species and mitochondrial superoxide in MC3T3-E1 cells. In addition, apocynin increased glutathione levels and restored the activity of glyoxalase I inhibited by MG. These findings suggest that apocynin provide a protective action against MG-induced cell damage by reducing oxidative stress and by increasing the MG detoxification system. Apocynin treatment decreased the levels of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6 induced by MG. Additionally, the nitric oxide level reduced by MG was significantly increased by apocynin. These findings indicate that apocynin might exert its therapeutic effects via upregulation of glyoxalase system and antioxidant activity. Taken together, apocynin may prove to be an effective treatment for diabetic osteopathy. Copyright © 2014 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 07/2014; · 2.60 Impact Factor
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    ABSTRACT: Methylglyoxal (MG) has been suggested to be one major source of intracellular reactive carbonyl compounds. In the present study, the effect of paeoniflorin on MG-induced cytotoxicity was investigated using osteoblastic MC3T3-E1 cells.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 06/2014; · 2.97 Impact Factor
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    ABSTRACT: Methylglyoxal (MG), a reactive dicarbonyl compound, is a metabolic byproduct of glycolysis and elevated MG levels contribute to diabetic complications. Glycation reactions of MG with amino acids can induce oxidative stress, leading to subsequent cytotoxicity. In the present study, the effect of liquiritigenin on MG-induced cytotoxicity was investigated using osteoblastic MC3T3-E1 cells. Pretreatment of MC3T3-E1 cells with liquiritigenin prevented the MG-induced cell death and production of protein adduct, intracellular reactive oxygen species, mitochondrial superoxide, cardiolipin peroxidation, and TNF-α in osteoblastic MC3T3-E1 cells. In addition, liquiritigenin increased the activity of glyoxalase I inhibited by MG. These findings suggest that liquiritigenin provides a protective action against MG-induced cell damage by reducing oxidative stress and by increasing MG detoxification. Pretreatment with liquiritigenin prior to MG exposure reduced MG-induced mitochondrial dysfunction by preventing mitochondrial membrane potential dissipation and adenosine triphosphate loss. Additionally, the nitric oxide and PGC-1α levels were significantly increased by liquiritigenin, suggesting that liquiritigenin may induce mitochondrial biogenesis. Our findings indicate that liquiritigenin might exert its therapeutic effects via enhancement of glyoxalase I activity and mitochondrial function, and anti-oxidant and anti-inflammatory activities. Taken together, liquiritigenin has potential as a preventive agent against the development of diabetic osteopathy related to MG-induced oxidative stress in diabetes.
    Food & function. 05/2014;
  • Young Soon Lee, Eun Mi Choi
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    ABSTRACT: Abstract Actein, isolated from black cohosh, was subjected to in vitro experiments to investigate its functional bioactivities in osteoblastic MC3T3-E1 cells. Actein caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, mineralization, and glutathione content in the cells, suggesting that actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis. We investigated the protective effects of actein on mitochondrial electron transport inhibitor, antimycin A induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant decrease in cell viability and mineralization. However, pretreatment with actein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, cardiolipin oxidation, ROS release, and nitrotyrosine increase, suggesting that actein may be useful for protecting mitochondria against a burst of oxidative stress. In addition, actein increased the phosphorylation of CREB (cAMP-response element-binding protein) inhibited by antimycin A and decreased the production of TNF-α induced by antimycin A. These findings suggest that actein could prevent oxidative damage to osteoblasts in osteoporotic patients.
    Journal of medicinal food 02/2014; · 1.39 Impact Factor
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    ABSTRACT: Abstract Methylglyoxal is a reactive dicarbonyl compound produced by glycolytic processing and identified as a precursor of advanced glycation end products. The elevated methylglyoxal levels in patients with diabetes are believed to contribute to diabetic complications, including bone defects. The objective of this study was to evaluate the effect of methylglyoxal on the function of osteoblastic MC3T3-E1 cells. The data indicated that methylglyoxal decreased osteoblast differentiation and induced osteoblast cytotoxicity. Pretreatment of MC3T3-E1 cells with aminoguanidine (a carbonyl scavenger), Trolox (an antioxidant), and cyclosporin A (a blocker of the mitochondrial permeability transition pore) prevented methylglyoxal-induced cytotoxicity in MC3T3-E1 cells. However, BAPTA/AM (an intracellular Ca(2+) chelator) and dantrolene (an inhibitor of endoplasmic reticulum Ca(2+) release) did not reverse the cytotoxic effect of methylglyoxal. Methylglyoxal increased the formation of intracellular reactive oxygen species, mitochondrial superoxide, and cardiolipin peroxidation in osteoblastic MC3T3-E1 cells. Methylglyoxal also decreased the mitochondrial membrane potential and intracellular ATP and nitric oxide levels, suggesting that carbonyl stress-induced loss of mitochondrial integrity contributes to the cytotoxicity of methylglyoxal. Furthermore, the results demonstrated that methylglyoxal induced protein adduct formation, inactivation of glyoxalase I, and activation of glyoxalase II. Aminoguanidine reversed all aforementioned effects of methylglyoxal. Taken together, these data support the notion that high methylglyoxal concentrations have detrimental effects on osteoblasts through a mechanism involving oxidative stress and mitochondrial dysfunction.
    Free Radical Research 10/2013; · 3.28 Impact Factor
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    ABSTRACT: Achyranthes bidentata (A. bidentata) Blume is a medicinal herb with the property of strengthening bones and muscles and ensuring proper downward flow of blood in terms of the therapeutic theory of traditional medicine. In the present study, the effect of A. bidentata root extract (AE) on osteoblast function was investigated in osteoblastic MC3T3-E1 cells. AE caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, and mineralization in the cells (P < 0.05). AE also decreased the production of TNF-α, IL-6, and RANKL induced by antimycin A, mitochondrial electron transport inhibitor. Exposure of MC3T3-E1 cells to antimycin A caused significant reduction of cell viability and mineralization. However, pretreatment with AE prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, ATP loss, ROS release, and nitrotyrosine increase, suggesting that AE may be useful for protecting mitochondria against a burst of oxidative stress. Moreover, AE increased the phosphorylation of cAMP-response element-binding protein inhibited by antimycin A. Our study demonstrates that A. bidentata could significantly prevent osteoblast damage in aged patients.
    Cytotechnology 10/2013; · 1.32 Impact Factor
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    ABSTRACT: We investigated the protective effect of liquiritigenin, one of the flavonoids present in Glycyrrhizae radix, against antimycin A-induced mitochondrial dysfunction in MC3T3-E1 osteoblast cells. Osteoblastic MC3T3-E1 cells were pre-incubated with liquiritigenin before treatment with antimycin A, and markers of mitochondrial function and oxidative damage were examined. In addition, the effects of liquiritigenin on the activation of phosphoinositide 3-kinase (PI3K) were examined in MC3T3-E1 cells. Liquiritigenin protected MC3T3-E1 cells from antimycin A-induced cell death. However, the PI3K inhibitor, LY294002, significantly attenuated liquiritigenin-mediated cell survival, indicating the involvement of PI3K in the cytoprotective effect of liquiritigenin. Pretreatment with liquiritigenin prior to antimycin A exposure significantly reduced antimycin A-induced PI3K inactivation, mitochondrial membrane potential dissipation, complex IV inactivation, and ATP loss. Liquiritigenin also reduced mitochondrial superoxide generation, nitrotyrosine production, and cardiolipin peroxidation during mitochondrial complex inhibition with antimycin A. Taken together, the results of this study show that modulation of PI3K, antioxidant effects, and the attenuation of mitochondrial dysfunction by liquiritigenin represent an important mechanism for its protection of osteoblasts against cytotoxicity resulting from mitochondrial oxidative stress. Copyright © 2013 John Wiley & Sons, Ltd.
    Phytotherapy Research 10/2013; · 2.07 Impact Factor
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    ABSTRACT: RANKL has been shown to play a critical role in osteoclast formation and bone resorption. Thus, agents that suppress RANKL signaling have a potential to suppress bone loss. In this study, we examined the ability of xanthohumol, a structurally simple prenylated chalcone, to suppress RANKL signaling during osteoclastogenesis in RAW264.7 cells. Xanthohumol markedly inhibited RANKL-induced TRAP activity, multinucleated osteoclasts formation, and resorption-pit formation. In experiments to elucidate its mechanism of action, xanthohumol was found to suppress RANKL-induced expression of TRAF6, GAB2, ERK, c-Src, PI3K, and Akt genes. Moreover, RANKL-induced expressions of c-Fos and NFATc1, which are crucial transcription factors for osteoclastogenesis, were reduced by treatment with xanthohumol. Xanthohumol also inhibited RANKL-induced expression of bone-resorption related osteoclast-specific genes (carbonic anhydrase II, TCIRG, CLCN7, OSTM1, cathepsin K, and MMP-9). These data demonstrate that xanthohumol inhibits osteoclastogenesis by modulating RANKL signaling and may be useful for the prevention of bone-destructive diseases such as osteoporosis, arthritis and periodontitis.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 08/2013; · 2.99 Impact Factor
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    ABSTRACT: Zinc oxide nanoparticles (ZnO NPs) can be ingested directly when used in food, food packaging, drug delivery, and cosmetics. This study evaluated the cellular effects of ZnO NPs (50 and 100 nm diameter particle sizes) on the function of osteoblastic MC3T3-E1 cells. ZnO NPs showed cytotoxicity at concentrations of above 50 μg/ml, and there was no significant effect of the size on the cytotoxicity of ZnO NPs. Within the testing concentrations of 0.01∼1 μg/ml, which did not cause a marked drop in cell viability, ZnO NPs (0.1 μg/ml) caused a significant elevation of alkaline phosphatase activity, collagen synthesis, mineralization, and osteocalcin content in the cells (P < 0.05). Moreover, pretreatment with ZnO NPs (0.01∼1 μg/ml) significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, and ATP loss. Measurement of reactive oxygen species (ROS) indicated decrease in ROS level upon exposure to ZnO nanoparticles (0.01 μg/ml). Hence, our study indicated that ZnO nanoparticles can have protective effects on osteoblasts at low concentrations where there are little or no observable cytotoxic effects.
    Biological trace element research 08/2013; · 1.92 Impact Factor
  • Eun Mi Choi, Young Soon Lee
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    ABSTRACT: The protective effects of paeoniflorin isolated from Paeonia lactiflora against pharmacological inhibition of the respiratory chain were studied using osteoblastic MC3T3-E1 cells. Here we show that paeoniflorin decreases cell death induced by antimycin A, an inhibitor of mitochondrial complex III. Paeoniflorin restored antimycin A-induced inactivation of phosphoinositide 3-kinase (PI3K) and thioredoxin reductase, suggesting that PI3K and thioredoxin reductase may be involved in paeoniflorin-induced cytoprotective responses. We also examined the effect of paeoniflorin on mitochondrial dysfunction and oxidative stress induced by antimycin A. Paeoniflorin inhibited mitochondrial membrane potential dissipation, ATP loss, inactivation of complexes I and IV, cytochrome c release, and cardiolipin oxidation induced by antimycin A. In addition, paeoniflorin prevented antimycin A-induced ROS release and nitrotyrosine increase. These results imply that paeoniflorin protects osteoblasts from antimycin A-induced cell death via improved mitochondrial function.
    Food & function. 07/2013;
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    ABSTRACT: Albiflorin isolated from Paeoniae Radix was investigated for its ability to protect against antimycin A-induced osteoblast toxicity in the MC3T3-E1 cell line. MC3T3-E1 cells showed significantly reduced viability, increased apoptosis and lactate dehydrogenase release, elevated ROS/RNS levels, and decreased mitochondrial function after exposure to antimycin A. Pretreatment with albiflorin reversed the loss of cell viability in antimycin A-treated cultures. Similarly, pretreatment with albiflorin before antimycin A resulted in decreased apoptosis and lactate dehydrogenase release, decreased ROS/RNS levels, and increased mitochondrial function compared to antimycin A-treated cultures. In addition, albiflorin increased the mineralization reduced by antimycin A. Albiflorin reduced antimycin A-induced mitochondrial cytochrome c loss and cardiolipin peroxidation, conferring protection against ROS. These results confirmed the crucial role of cytochrome c and cardiolipin in the underlying mechanistic action of albiflorin. Therefore, the results suggest that albiflorin enhances mitochondrial function to suppress antimycin A-induced oxidative damage via the preservation of cytochrome c and cardiolipin. All of these data indicate that albiflorin may reduce or prevent osteoblast degeneration in osteoporosis.
    Fitoterapia 05/2013; · 2.23 Impact Factor
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    ABSTRACT: Gold nanoparticles have shown promising biological applications due to their unique properties. Understanding the interaction mechanisms between nanomaterials and biological cells is important for the control and manipulation of these interactions for biomedical applications. In the present study, we investigated the effects of gold nanoparticles on the differentiation of osteoblastic MC3T3-E1 cells and antimycin A-induced mitochondrial dysfunction. The results showed that gold nanoparticles (5, 10, and 20 nm) caused a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, and osteocalcin content in the cells (P < 0.05). Moreover, pretreatment with gold nanoparticles prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, cytochrome c release, cardiolipin peroxidation, and reactive oxygen species generation. Taken together, our study indicated that gold nanoparticles may improve the differentiation and have protective effects on mitochondrial dysfunction of osteoblastic cells.
    Biological trace element research 05/2013; · 1.92 Impact Factor
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    ABSTRACT: Age-related osteoblast dysfunction is the main cause of agerelated bone loss in both men and women. In the present study, the effect of sciadopitysin, a type of biflavonoids, on osteoblast function was investigated in osteoblastic MC3T3-E1 cells. Sciadopitysin caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, mineralization, and glutathione content in the cells (P<0.05). Sciadopitysin also decreased the production of tumor necrosis factor-a (TNF-α) induced by antimycin A, a mitochondrial electron transport inhibitor. We investigated the protective effects of sciadopitysin on antimycin A-induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused a significant reduction in osteoblast dysfunction. However, pretreatment with sciadopitysin prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, adenosine triphosphate (ATP) loss, reactive oxygen species (ROS) release, and nitrotyrosine increase, suggesting that sciadopitysin may be useful for protecting mitochondria against a burst of oxidative stress. Moreover, sciadopitysin increased phosphorylation of cAMP-response element-binding protein (CREB) inhibited by antimycin A. Our results demonstrate that sciadopitysin may reduce or prevent osteoblasts degeneration.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 04/2013; · 2.99 Impact Factor
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    ABSTRACT: Abstract This study examined the effect of pinacidil, a nonselective adenosine triphosphate-sensitive potassium channel opener, on the function of osteoblastic MC3T3-E1 cells. Pinacidil caused a significant elevation of collagen synthesis, alkaline phosphatase activity, osteocalcin synthesis and mineralization in the cells (p < 0.05). Pinacidil significantly decreased the production of osteoclast differentiation inducing factors such as TNF-α, IL-6 and receptor activator of nuclear factor-κB ligand in the presence of antimycin A, which inhibits mitochondrial electron transport. Moreover, pinacidil prevented antimycin A-induced reactive oxygen species and nitrotyrosine production. These results demonstrate that pinacidil may have positive effects on skeletal structure.
    Immunopharmacology and Immunotoxicology 03/2013; · 1.36 Impact Factor
  • Eun Mi Choi
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    ABSTRACT: The protective effect of quercitrin on the response of osteoblastic MC3T3-E1 cells to oxidative stress was evaluated. Osteoblasts were incubated with H(2)O(2) and/or quercitrin, and markers of osteoblast function and oxidative damage were examined. Quercitrin treatment reversed the cytotoxic effect of H(2)O(2) significantly (P<0.05). This effect was blocked by ICI182780 and LY294002, suggesting that quercitrin's effect might be involved in estrogen action and results from PI3K mediated signaling pathway. Pretreatment of quercitrin increased collagen content, alkaline phosphatase (ALP) activity, and calcium deposition of osteoblasts compared with H(2)O(2) treated cells and these effects were blocked by ERKs and p38 mitogen-activated protein kinases (MAPKs) inhibitors such as PD98059 and SB203580, respectively. These suggest that quercitrin-induced protective effect against osteoblast dysfunction by oxidative stress is associated with increased activation of ERKs and p38 MAPK. Pretreatment with quercitrin also reduced the increase in bone-resorbing factor, receptor activator of nuclear factor-kB ligand (RANKL) and oxidative damage markers (malondialdehyde, protein carbonyl, and nitrotyrosine) induced by H(2)O(2). These results suggest that quercitrin may be protective against H(2)O(2)-induced dysfunction in osteoblasts.
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 03/2012; 64(3):211-6. · 1.43 Impact Factor
  • Min Su Seo, Eun Mi Choi
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    ABSTRACT: Antimycin A (AMA) inhibits mitochondrial electron transport chain between cytochrome b and c. In the present study, we investigated the effects of dehydrocostus lactone on osteoblastic MC3T3-E1 cells in the presence of AMA with a focus on redox changes and PI3K/Akt/CREB signaling. AMA increased nitrotyrosin level and decreased NADPH level, activities of thioredoxin reductase, phosphoinositide 3-kinase (PI3K), and Akt (protein kinase B [PKB]), and phosphorylated cAMP-response element-binding protein (CREB). Pretreatment with dehydrocostus lactone prior to AMA exposure significantly prevented the loss of NADPH, production of nitrotyrosine, and thioredoxin reductase inactivation induced by AMA. Moreover, dehydrocostus lactone increased activities of PI3K and Akt, and CREB phosphorylation inhibited by AMA. These results suggest that antioxidant activity and PI3K/Akt/CREB activation are related to the protective effect of dehydrocostus lactone against osteoblast damage induced by AMA.
    Immunopharmacology and Immunotoxicology 02/2012; 34(5):810-4. · 1.36 Impact Factor
  • Eun Mi Choi
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    ABSTRACT: Antimycin A treatment of cells blocks the mitochondrial electron transport chain and leads to elevated ROS generation. In the present study, we investigated the protective effects of magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, on antimycin A-induced toxicity in osteoblastic MC3T3-E1 cells. Osteoblastic MC3T3-E1 cells were pre-incubated with magnolol before treatment with antimycin A. Cell viability and mineralization of osteoblasts were assessed by MTT assay and Alizarin Red staining, respectively. Mitochondrial dysfunction in cells was measured by mitochondrial membrane potential (MMP), complex IV activity, and ATP level. The cellular antioxidant effect of magnolol in osteoblastic MC3T3-E1 cells was assessed by measuring cardiolipin oxidation, mitochondrial superoxide levels, and nitrotyrosine content. Phosphorylated cAMP-response element-binding protein (CREB ) was evaluated using ELISA assay. Pretreatment with magnolol prior to antimycin A exposure significantly reduced antimycin A-induced osteoblast dysfunction by preventing MMP dissipation, ATP loss, and CREB inactivation. Magnolol also reduced cardiolipin peroxidation, mitochondrial superoxide, and nitrotyrosine production induced by antimycin A. These results suggest that magnolol has a protective effect against antimycin A-induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. All these data indicate that magnolol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders.
    Inflammation 01/2012; 35(3):1204-12. · 2.46 Impact Factor
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    ABSTRACT: In the present study, the ability of magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, to stimulate osteoblast function and inhibit the release of bone-resorbing mediators was investigated in osteoblastic MC3T3-E1 cells. Osteoblast function was measured by cell growth, alkaline phosphatase activity, collagen synthesis, and mineralization. Glutathione content was also measured in the cells. Bone-resorbing cytokines, receptor activator of nuclear factor-κB ligand (RANKL), TNF-α, and IL-6 were measured with an enzyme immunoassay system. Magnolol caused a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, and glutathione content in the cells (P < 0.05). Skeletal turnover is orchestrated by a complex network of regulatory factors. Among cytokines, RANKL, TNF-α, and IL-6 were found to be key osteoclastogenetic molecules produced by osteoblasts. Magnolol significantly (P < 0.05) decreased the production of osteoclast differentiation inducing factors such as RANKL, TNF-α, and IL-6 in the presence of antimycin A, which inhibits mitochondrial electron transport and has been used as an ROS generator. Magnolol might be a candidate as an agent for the prevention of bone disorders such as osteoporosis.
    Mediators of Inflammation 01/2012; 2012:829650. · 3.88 Impact Factor
  • Eun Mi Choi
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    ABSTRACT: Osteoporosis is recognised as one of the major hormonal deficiency diseases, especially in menopausal women and the elderly. The present study investigated whether treatment with sunflower (Helianthus annuus L.) seed extract (SSE) may affect the function of MC3T3-E1 osteogenic cells. In order to determine the growth and differentiation of osteoblast, MTT (3-(4,5-dimethyl-thiazol-2yl)-2,5-diphenyl tetrazolium bromide) assay, alkaline phosphatase (ALP) activity, collagen synthesis and osteocalcin secretion were performed. Also, the production of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and nitric oxide (NO) in osteoblastic MC3T3-E1 cells was measured. SSE significantly (p
    Food and Agricultural Immunology 01/2012; · 0.73 Impact Factor
  • Eun Mi Choi
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    ABSTRACT: Deoxyactein is one of the major constituents isolated from Cimicifuga racemosa. In the present study, we investigated the protective effects of deoxyactein on antimycin A (mitochondrial electron transport inhibitor)-induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant cell viability loss, as well as mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, intracellular calcium ([Ca(2+) ](i) ) elevation and oxidative stress. Pretreatment with deoxyactein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, ATP loss, [Ca(2+) ](i) elevation and oxidative stress. Moreover, deoxyactein increased the activation of PI3K (phosphoinositide 3-kinase), Akt (protein kinase B) and CREB (cAMP-response element-binding protein) inhibited by antimycin A. All these data indicate that deoxyactein may reduce or prevent osteoblasts degeneration in osteoporosis or other degenerative disorders. Copyright © 2011 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 12/2011; · 2.60 Impact Factor

Publication Stats

389 Citations
160.55 Total Impact Points

Institutions

  • 2010–2014
    • Kyung Hee University
      • Department of Food and Nutrition
      Sŏul, Seoul, South Korea
  • 2013
    • Kyung Hee University Medical Center
      • Department of Endocrinology and Metabolism
      Sŏul, Seoul, South Korea
  • 2012
    • Yeungnam University
      Onyang, South Chungcheong, South Korea
  • 2008–2011
    • Chungnam National University
      • College of Pharmacy
      Seongnam, Gyeonggi, South Korea
    • University of Ulsan
      • The Immunomodulation Research Center
      Ulsan, Ulsan, South Korea
  • 2009
    • Kangwon National University Hospital
      Shunsen, Gangwon, South Korea
  • 2008–2009
    • Duksung Women's University
      Sŏul, Seoul, South Korea
  • 2007–2008
    • Vietnamese Academy of Science and Technology Institute of Information Technology
      Hà Nội, Ha Nội, Vietnam
  • 2003–2005
    • Pohang University of Science and Technology
      • Department of Physics
      Andong, North Gyeongsang, South Korea