• Title/Summary/Keyword: Biomaterial

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Initial tissue response of biodegradable membrane in rat subcutaneous model (백서 피하층에서 흡수성 차단막의 초기 조직 반응)

  • Lim, Hyun-Chang;Chae, Gyung-Joon;Jung, Ui-Won;Kim, Chang-Sung;Lee, Yong-Keun;Cho, Kyoo-Sung;Kim, Chong-Kwan;Choi, Seong-Ho
    • Journal of Periodontal and Implant Science
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    • v.37 no.4
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    • pp.839-848
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    • 2007
  • Purpose: Various kinds of biodegradable membranes are currently used in dental clinics. And the frequency and the necessity of their usage are increasing due to their numerous advantages. Therefore it is important to understand the difference of various membranes and histological reaction against implanted membranes. Materials and Methods: Biodegradable membranes of $Biogide^{(R)}$, $Resolute^{(R)}$, and $Tutodent^{(R)}$ were cut into small pieces by $1.0{\times}0.5cm$. The membranes were implanted 1.5cm apart from each other under the epithelium on the skull of 18 Sprague Dawley rats. The animals were sacrificed at 3, 7, and 14 days after surgical procedure. The specimens were examined by histological analysis. Results: 1. Early period after implantation of the membranes showed connective tissues surrounding membranes and there were a few inflammatory cells present. 2. In $Biogide^{(R)}$ and $Tutodent^{(R)}$ specimens, inflammatory cells and surrounding tissues were shown to infiltrate from outside with slight density difference inside. In $Resolute^{(R)}$ specimens, membranes were fragmented. Inflammatory cells and connective tissues were also observed inside. 3. In $Resolute^{(R)}$ specimen, giant cells were present which implicates that foreign body reaction has occurred. 4. $Biogide^{(R)}$ had lower integrity than other membranes and is not enough to be used alone in defect area. However, $Resolute^{(R)}$ had superior firmness than others. $Tutodent^{(R)}$ had middle level of integrity. Conclusion: This experimental model enabled to observe early inflammatory reactions and morphological changes of materials and can be used to develop and evaluate the efficacy of biodegradable membranes. Duplication of standardized human oral environment will be required in future experiments.

The effects of novel biodegradable amorphous Calcium Phosphate on bone regeneration in rat calvarial defects (새롭게 개발된 비정질의 Calcium Phosphate가 백서두개골의 골재생에 미치는 영향)

  • Choi, Jung-Yoo;Chae, Gyung-Joon;Kim, Chang-Sung;Lee, Yong-Keun;Cho, Kyoo-Sung;Chai, Joong-Kyu;Kim, Chong-Kwan;Choi, Seong-Ho
    • Journal of Periodontal and Implant Science
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    • v.37 no.4
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    • pp.871-879
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    • 2007
  • Purpose: The purpose of this study was to evaluate the bone regeneration of novel biodegradable amorphous calcium phosphate. Materials and Method: An 8-mm, calvarial, critical-size osteotomy defect was created in each of 20 male Sprague-Dawley rats(weight $250{\sim}300g$). The animals were divided into two groups of 10 animals each and allowed to heal for 2 weeks(10 rats). The first group was the control group and the other group was the experimental group which received the novel biodegradable calcium phosphate. Results: The healing of the calvarium in the control group was uneventful. The histologic results showed little bone formation in the control group. The experimental group which received the novel biodegradable calcium phosphate showed a normal wound healing. There were a lot of new bone formation around the biomaterial in 2 weeks. The bone formation increased in 8 weeks when compared to 2 weeks and there was a significant bone increase as well(P<0.01). The nobel biodegradable calcium phosphate showed statistical significance when compared to the control group (P<0.05). The novel biodegradable calcium phosphate in 8 weeks showed a significant increase in bone formation when compared to 2 weeks $(40.4{\pm}1.6)$(%). The biodegradable calcium phosphate which is made from mixing calcium phosphate glass(CPG), NaCO and NaOH solution, is biocompatible, osteoconductive and has a high potency of bone formation. Conclusion: We can conclude that the novel biodegradable calcium phosphate can be used as an efficient bone graft material for its biodegradability and osteoconductivity.

Sustained Release of Proteins Using Small Intestinal Submucosa Modified PLGA Scaffold (SIS로 개질된 PLGA 담체에서의 단백질의 서방화)

  • Ko, Youn-Kyung;Choi, Myung-Kyu;Kim, Soon-Hee;Kim, Geun-Ah;Lee, Hai-Bang;Rhee, John-M.;Khang, Gil-Son
    • Polymer(Korea)
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    • v.32 no.3
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    • pp.199-205
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    • 2008
  • In this study, we fabricated poly (lactide-co-glycolide) (PLGA) scaffold modified with small intestinal submucosa (SIS) as a drug delivery matrix of bioactive molecules. SIS derived from the submucosa layer of porcine intestine has been widely used as biomaterial because of low immune response. PLGA scaffold was prepared by the method of solvent casting/salt leaching. Novel composite scaffolds of SIS/PLGA were manufactured by simple immersion method of PLGA scaffold in SIS solution under vacuum. SEM observation shows that PLGA and SIS/PLGA scaffolds have interconnective and open pores. Especially, SIS/PLGA scaffold showed that micro-sponge of SIS with interconnected pore structures were formed in the pores of PLGA scaffold. In order to assay release profile of proteins, we manufactured FITC conjugated BSA loaded PLGA and SIS/PLGA scaffold. And the release amount was identified by fluorescence intensity using the fluorescence spectrophotometer. The initial burst of BSA containing SIS/PLGA scaffolds was lower than that of PLGA scaffolds resulting in constant release. And release of BSA in SIS/PLGA scaffold was fast and incremental because of the increased content of BSA. In conclusion, we confirmed that penetrated SIS solution prevented the initial burst of BSA and PLGA modified with SIS scaffold is useful as protein carriers with controlled release pattern.

Induction of G2/M Arrest of the Cell Cycle by Genistein in Human Bladder Carcinoma and Leukemic Cells (인체 방광암 및 백혈병세포에서 genistein에 의한 세포주기 G2/M arrest 유발에 관한 연구)

  • Kim, Eu-Kyum;Myong, You-Ho;Song, Kwan-Sung;Lee, Ki-Hong;Rhu, Chung-Ho;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.16 no.4
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    • pp.589-597
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    • 2006
  • Genistein, a natural isoflavonoid phytoestrogen, is a strong inhibitor of protein tyrosine kinase and DNA topoisomerase activities. There are several studies documenting molecular alterations leading to cell cycle arrest and induction of apoptosis by genistein as a chemopreventive agent in a variety of cancer cell lines; however, its mechanism of action and its molecular targets on human bladder carcinoma and leukemic cells remain unclear. In the present study, we have addressed the mechanism of action by which genistein suppressed the proliferation of T24 bladder carcinoma and U937 leukemic cells. Genistein significantly inhibited the cell growth and induced morphological changes, and induced the G2/M arrest of the cell cycle in both T24 and U937 cells with a relatively stronger cytotoxicity in U937. The G2/M arrest in T24 cells was associated with the inhibition of cyclin A, cyclin B1 and Cdc25C protein expression without alteration of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21(WAF1/CIP1). However, the inhibitory effects of genistein on the cell growth of U937 cells were connected with a marked inhibition of cyclin B1 and an induction of Cdk inhibitor p21 proteins by p53-independent manner. These data suggest that genistein may exert a strong anticancer effect and additional studies will be needed to evaluate the different mechanisms between T24 and U937 cells.

Regulation of Cyclin D3 by Calpain Protease in Human Breast Carcinoma MDA-MB-231 Cells (인체 유방암세포에서 calpain protease에 의한 cyclin D3의 발현 조절)

  • Choi, Byung-Tae;Kim, Gun-Do;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.16 no.4
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    • pp.598-604
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    • 2006
  • The $Ca^{2+}-activated$ neutral protease calpain induced proteolysis has been suggested to play a role in certain cell growth regulatory proteins. Cyclin proteolysis is essential for cell cycle progression. D-type cyclins, which form an assembly with cyclin-dependent kinases (cdk4 and cdk6), are synthesized earlier in G1 of the cell cycle and seem to be induced in response to external signals that promote entry into the cell cycle. Here we show that cyclin D3 protein levels are regulated at the posttranscriptional level by calpain protease. Treatment of human breast carcinoma MDA-MB-231 cells with lovastatin and actinomycin D resulted in a loss of cyclin D3 protein that was completely reversible by the peptide aldehyde calpain inhibitor, LLnL. The specific inhibitor of the 26S proteasome, lactacystin, the lysosome inhibitors, ammonium chloride and chloroquine, and the serine protease inhibitor, phenylmethylsulfonylfluoride (PMSF), did not block the degradation of cyclin D3 by lovastatin and actinomycin D. Results of in vitro degradation of cyclin D3 by purified calpain showed that cyclin D3 protein is degraded in a $Ca^{2+}-dependent$ manner, and the half-life of cyclin D3 protein was dramatically increased in LLnL treated cells. These data suggested that cyclin D3 protein is regulated by the $Ca^{2+}-activated$ protease calpain.

Modulation of Cell Cycle Regulators by Sulforaphane in Human Mepatocarcinoma HepG2 Cells (HepG2 인체간암세포의 세포주기조절인자 발현에 미치는 sulforaphane의 영향)

  • Bae, Song-Ja;Kim, Gi-Young;Yoo, Young-Hyun;Choi, Byung-Tae;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.16 no.7 s.80
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    • pp.1235-1242
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    • 2006
  • Sulforaphane, an isothiocyanate derived from hydrolysis of glucoraphanin in broccoli and other cruciferous vegetables, was shown to induce phase II detoxification enzymes and inhibit chemically induced mammary tumors in rodents. Recently, sulforaphane is known to induce cell cycle arrest and apoptosis in human canter cells, however its molecular mechanisms are poorly understood. In tile present study, we demonstrated that sulforaphane acted to inhibit proliferation and induce morphological changes of human hepatocarcinoma HepG2 cells. Treatment of HepG2 cells with $10{\mu}M\;or\;15{\mu}M$ sulforaphane resulted in significant G2/M cell cycle arrest as determined by DNA flow cytometry. Moreover, $20{\mu}M$ sulforaphane significantly induced the population of sub-G1 cells suggesting that sulforaphane induced apoptosis. This anti-proliferative effect of sulforaphane was accompanied by a marked inhibition of ryclin A, cyclin 31 and Cdc2 protein. However, the levels of tumor suppressor p53 and Cdk inhibitor p21 mRNA and protein expression were significantly increased by sulforaphane treatment in a concentration-dependent manner. Although further studies are needed, the present work suggests that sulforaphane may be a potential rhemoprevetiveichemotherapeucc agent for the treatment of human cancer cells.

Ginseng Saponin-Re and Coix lachrymajobi var. mayuen Regulate Obesity Related Genes Expressions, TNF-alpha, Leptin, Lipoprotein Lipase and Resistin in 3T3-L1 Adipocytes (지방세포 3T3-L1에 인삼 사포닌 Re와 의이인 추출액 처리시 비만관련 유전자인 TNF-α, lipoprotein lipase, leptin 및 resistin 발현 조절에 미치는 영향)

  • Kim, Sung-Ok
    • Journal of Life Science
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    • v.17 no.11
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    • pp.1523-1532
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    • 2007
  • In order to determine if the mRNA and protein expression levels of 3T3-L1 adipocytes are influenced by oriental medicines, adipocytes were treated with $100\;{\mu}g/ml$ of G-Re and aqueous extract of a Coix lachrymajobi var. mayuen (AEC) every other day for 12 days, respectively. The tumor necrosis factor alpha ($TNF-{\alpha}$). mRNA and protein expressions were suppressed markedly in treated mature adipocytes. Those of lipoprotein lipase (LPL) levels were found to increase gradually in preadipocytes differentiating into mature adipocytes. Those were higher than that of the untreated mature adipocytes. The treated adipocytes showed reduction of leptin expression levels, while in untreated mature adipocytes cell, those of levels were significantly higher after the conversion of preadipocytes into mature adipocytes. The resistin levels in the treated adipocytes were significantly decreased comparing to that of the untreated mature adipocytes. In conclusion, the expression levels of LPL, $TNF-{\alpha}$, leptin and resistin mRNA and proteins are shown to be regulated by G-Re and AEC, making them potential candidates for controlling fat mass related obesity.

Improvement of High-fat Diet-induced Obesity by Xanthigen in C57BL/6N Mice (잔티젠(Xanthigen)에 의한 고지방식이로 유도된 비만 개선 효과)

  • Choi, Kyeong-Mi;Lee, Youn-Sun;Kim, Wonkyun;Choi, Yung-Hyun;Kwak, Youn-Gil;Jung, Jae-Chul;Lee, Jeongrai;Yoo, Hwan-Soo
    • Journal of Life Science
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    • v.22 no.12
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    • pp.1697-1703
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    • 2012
  • Obesity is a risk factor for numerous metabolic diseases. Recently, naturally occurring compounds that may improve obesity have received increasing attention. Xanthigen is a mixture of fucoxanthin and punicic acid derived from brown seaweed and pomegranate seed, respectively, which have been traditionally used for lipid-lowering effects in humans. In this study, we investigated whether Xanthigen attenuates high-fat diet-induced obesity in C57BL/6N mice. The mice were fed on a normal diet (ND), high-fat diet (HFD), HFD plus 1% Xanthigen or HFD plus 1% green tea extract (GTE) for 11 weeks. Food efficiency ratio (FER) and body weight were significantly reduced in mice fed HFD plus Xanthigen compared to HFD-fed mice. Consistent with the results in body weight change, Xanthigen also significantly decreased the weights of epididymal adipose tissue, retroperitoneal adipose tissue, and liver in HFD plus 1% Xanthigen-fed mice. The serum level of low-density lipoprotein (LDL)-cholesterol was significantly decreased in HFD plus Xanthigen-fed mice compared to HFD-fed mice. These results suggest that Xanthigen may be useful in the development of a functional health food for anti-obesity.

G1 Arrest of U937 Human Monocytic Leukemia Cells by Sodium Butyrate, an HDAC Inhibitor, Via Induction of Cdk Inhibitors and Down-regulation of pRB Phosphorylation (Cdk inhibitors의 발현 증가 및 pRB 인산화 저해에 의한 HDAC inhibitor인 sodium butyrate에 의한 인체백혈병세포의 G1 arrest유발)

  • Choi, Yung-Hyun
    • Journal of Life Science
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    • v.19 no.7
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    • pp.871-877
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    • 2009
  • We investigated the effects of sodium butyrate, a histone deacetylase inhibitor, on the cell cycle progression in human monocytic leukemia U937 cells. Exposure of U937 cells to sodium butyrate resulted in growth inhibition, G1 arrest of the cell cycle and induction of apoptosis in a dose-dependent manner as measured by MTT assay and flow cytometry analysis. The increase in G1 arrest was associated with the down-regulation in cyclin D1, E, A, cyclin-dependent kinase (Cdk) 4 and 6 expression, and up-regulation of Cdk inhibitors such as p21 and p27. Sodium butyrate treatment also inhibited the phosphorylation of retinoblastoma protein (pRB) and p130, however, the levels of transcription factors E2F-1 and E2F-4 were not markedly modulated. Furthermore, the down-regulation of phosphorylation of pRB and p130 by this compound was associated with enhanced binding of pRB and E2F-1, as well as p130 and E2F-4, respectively. Overall, the present results demonstrate a combined mechanism involving the inhibition of pRBjp130 phosphorylation and induction of Cdk inhibitors as targets for sodium butyrate that may explain some of its anti-cancer effects in U937 cells.

G1 Arrest of the Cell Cycle by Gomisin N, a Dibenzocyclooctadiene Lignan, Isolated from Schizandra chinensis Baill in Human Leukemia U937 Cells (오미자에서 분리된 dibenzocyclooctadiene lignan의 일종인 gomisin N에 의한 인체혈구암세포의 세포주기 G1 arrest 유발)

  • Park, Cheol;Hwang, Hye-Jin;Choi, Byung-Tae;Choi, Tae-Hyun;Kim, Byung-Woo;Choi, Young-Whan;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.20 no.7
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    • pp.977-982
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    • 2010
  • We investigated the anti-cancer effects of two dibenzocyclooctadiene lignans, gomisin A and gomisin N, isolated from Schizandra chinensis Baill, in human promyelocytic U937 cells. Gomisin N, but not gomisin A, inhibited cell growth in a concentration-dependent manner, which was associated with the induction of G1 arrest of the cell cycle. G1 arrest induced by gomisin N was correlated with down-regulation of cyclin E, cyclin-dependent kinase (Cdk) 2 and Cdk4, and a concomitant up-regulation of Cdk inhibitors such as p16 (INK4A) and p21 (WAF1/CIP1). Furthermore, gomisin N inhibited phosphorylation of retinoblastoma protein (pRB) and p130, and expression of transcription factor E2Fs. The results indicated that growth inhibition by gomisin N is related to cell cycle arrest at G1 in U937 cells and these findings suggest that gomisin N may be a useful chemotherapeutic agent.