간행물
International Journal of Oral Biology KCI 등재후보
- 발행기관 대한구강생물학회
- 자료유형 학술지
- 간기 계간
- ISSN 1226-7155 (Print)2287-6618 (Online)
- 수록기간 1977 ~ 2024
- 주제분류 의약학 > 치의학 의약학 분류의 다른 간행물
- 십진분류KDC 515DDC 610
권호리스트/논문검색
Vol. 38 No. 3 (2013년 9월) 6건
1.
2013.09
구독 인증기관 무료, 개인회원 유료
Periodontal inflammation increases the risk of tooth loss, particularly in cases where there is an associated loss of alveolar bone and periodontal ligament (PDL). Histological and morphometric evaluation of periodontal inflammation is difficult. Especially, the lengths of the periodontal ligament and interdental alveolar bone space have not been quan-tified. A quantitative imaging procedure applicable to an animal model would be an important clinical study. The purpose of this study was to quantify the loss of alveolar bone and perio-dontal ligament by evaluation with micro-computed tomo-graphy (micro-CT). Another purpose was to investigate diffe-rences in infections with systemic E. coli LPS and TNF-α on E. coli lipopolysaccharide (LPS) in loss of alveolar bone and periodontal ligament model on mice. This study showed that linear measurements of alveolar bone loss were repre-sented with an increasing trend of the periodontal ligament length and interdental alveolar process space. The effects of systemic E. coli LPS and TNF-α on an E. coli LPS-induced periodontitis mice model were investigated in this research. Loss of periodontal ligament and alveolar bone were eval-uated by micro-computed tomography (micro-CT) and cal-culated by the two- and three dimensional microstructure morphometric parameters. Also, there was a significantly increasing trend of the interdental alveolar process space in E. coli LPS and TNF-α on E. coli LPS compared to PBS. And E. coli LPS and TNF-α on E. coli LPS had a slightly increa-sing trend of the periodontal ligament length. The increa-sing trend of TNF-α on the LPS-induced mice model in this experiment supports the previous studies on the contribu-tion of periodontal diseases in the pathogenesis of systemic diseases. Also, our findings offer a unique model for the study of the role of LPS-induced TNF-α in systemic and chronic local inflammatory processes and inflammatory diseases. In this study, we performed rapidly quantification of the perio-dontal inflammatory processes and periodontal bone loss using micro-computed tomography (micro-CT) in mice.
4,000원
2.
2013.09
구독 인증기관 무료, 개인회원 유료
Bile acids and synthetic bile acid derivatives induce apop-tosis in various kinds of cancer cells and thus have anti-cancer properties. Recently, it has been suggested that autop-hagy may play an important role in cancer therapy. How-ever, few data are available regarding the role of autophagy in oral cancers and there have been no reports of autophagic cell death in OSCCs (oral squamous cell carcinoma cells) in-duced by HS-1200, a synthetic bile acid derivative. We thus examine whether HS-1200 modulates autophagy in OSCCs. Our findings indicate that HS-1200 has anticancer effects in OSCCs, and we observed in these cells that autophagic vacuoles were visible by monodansylcadaverine (MDC)and acridine orange staining. When we analyzed HS-1200-treated OSCC cells for the presence of biochemical markers, we observed that this treatment directly affects the conversion of LC-3II, degradation of p62/SQSTM1 and full-length beclin-1, clea-vage of ATG5-12 and the activation of caspase. An autop-hagy inhibitor suppressed HS-1200-induced cell death in OSCCs, confirming that autophagy acts as a pro-death signal in these cells. Furthermore, HS-1200 shows anticancer acti-vity against OSCCs via both autophagy and apoptosis. Our current findings suggest that HS-1200 may potentially cont-ribute to oral cancer treatment and thus provide useful infor-mation for the future development of a new therapeutic agent.
4,000원
3.
2013.09
구독 인증기관 무료, 개인회원 유료
We investigated the synergistic apoptotic effects of co- treatments with Chios gum mastic (CGM) and eugenol on G361 human melanoma cells. An MTT assay was cond-ucted to investigate whether this co-treatment efficiently reduces the viability of G361 cells compared with each single treatment. The induction and augmentation of apop-tosis were confirmed by DNA electrophoresis, Hoechst stai-ning, and analyses of DNA hypoploidy. Western blot ana-lysis and immunofluorescent staining were also performed to evaluate expression and translocation of apoptosis- related proteins following CGM and eugenol co-treatment. Proteasome activity and mitochondrial membrane potential (MMP) changes were also assayed.The results indicated that the co-treatment of CGM and eugenol induces multiple pa-thways and processes associated with an apoptotic response in G361 cells. These include nuclear condensation, DNA fragmentation, a reduction in MMP and proteasome acti-vity, an increase of Bax and decrease of Bcl-2, a decreased DNA content, cytochrome c release into the cytosol, the translocation of AIF and DFF40 (CAD) into the nucleus, and the activation of caspase-9, caspase-7, caspase-3, PARP and DFF45 (ICAD). In contrast, separate treatments of 40 µg/ml CGM or 300 µM eugenol for 24 hours did not induce apoptosis. Our present data thus suggest that a combination therapy of CGM and eugenol is a potential treatment strategy for human melanoma.
4,000원
4.
2013.09
구독 인증기관 무료, 개인회원 유료
Objective. To investigate the effects of the hypoxia inducible factor-1 (HIF-1) activation–mimicking agent cobalt chloride (CoCl2) on the osteogenic differentiation of human mesenchy-mal stem cells (hMSCs) and elucidate the underlying mole-cular mechanisms. Study design. The dose and exposure periods for CoCl2 in hMSCs were optimized by cell viability assays. After confirmation of CoCl2-induced HIF-1α and vas-cular endothelial growth factor expression in these cells by RT-PCR, the effects of temporary preconditioning with CoCl2 on hMSC osteogenic differentiation were evaluated by RT- PCR analysis of osteogenic gene expression, an alkaline phos-phatase (ALP) activity assay and by alizarin red S staining. Results. Variable CoCl2 dosages (up to 500 µM) and exposure times (up to 7 days) on hMSC had little effect on hMSC survival. After CoCl2 treatment of hMSCs at 100 µM for 24 or 48 hours, followed by culture in osteogenic differentiating media, several osteogenic markers such as Runx-2, osteocal-cin and osteopontin, bone sialoprotein mRNA expression level were found to be up-regulated. Moreover, ALP acti-vity was increased in these treated cells in which an accele-rated osteogenic capacity was also verified by alizarin red S staining. Conclusions. The osteogenic differentiation poten-tial of hMSCs could be preserved and even enhanced by CoCl2 treatment.
4,000원
5.
2013.09
구독 인증기관 무료, 개인회원 유료
Tumor necrosis factor alpha (TNFα) is a multifunctional inflammatory cytokine that regulates various cellular and bio-logical processes. Increased levels of TNFα have been im-plicated in a number of human diseases including diabetes and arthritis. Sympathetic nervous system stimulation via the beta2-adrenergic receptor (β2AR) in osteoblasts suppresses osteogenic activity. We previously reported that TNFα up- regulates β2AR expression in murine osteoblastic cells and that this modulation is associated with TNFα inhibition of osteoblast differentiation. In our present study, we explored whether TNFα induces β2AR expression in human osteo-blasts and then identified the downstream signaling path-way. Our results indicated that β2AR expression was increa-sed in Saos-2 and C2C12 cells by TNFα treatment, and that this increase was blocked by the inhibition of NF-κB acti-vation. Chromatin immunoprecipitation and luciferase reporter assay results indicated that NF-κB directly binds to its cog-nate elements on the β2AR promoter and thereby stimulates β2AR expression. These findings suggest that the activation of TNFα signaling in osteoblastic cells leads to an upregu-lation of β2AR and also that TNFα induces β2AR exp-ression in an NF-κB-dependent manner.
4,000원
6.
2013.09
구독 인증기관 무료, 개인회원 유료
Seung-Ho Ohk, Hyunjoo Jeong, Jong-Pill Kim, Yun-Jung Yoo, Jeong-Taeg Seo, Dong-Min Shin, Syng-Ill Lee
Xylitol is a sugar alcohol with a variety of functions including bactericidal and anticariogenic effects. However, the cellular mechanisms underlying the role of xylitol in bone metabolism are not yet clarified. In our present study, we exploited the physiological role of xylitol on osteoclast dif-ferentiation in a co-culture system of osteoblastic and RAW 264.7 cells. Xylitol treatment of these co-cultures reduced the number of tartrate-resistant acid phosphatase (TRAP)- positive multinucleated cells induced by 10 nM 1α,25(OH)2 D3 in a dose‐dependent manner. A cell viability test revea-led no marked cellular damage by up to 100 mM of xylitol. Exposure of osteoblastic cells to xylitol decreased RANKL, but not OPG, mRNA expression in the presence of 10-8 M 1α,25(OH)2D3 in a dose‐dependent manner. Furthermore, bone resorption activity, assessed on bone slices in the co- culture system, was found to be dramatically decreased with increasing xylitol concentrations. RANKL and OPG proteins were assayed by ELISA and the soluble RANKL (sRANKL) concentration was decreased with an increased xylitol con-centration. In contrast, OPG was unaltered by any xylitol con-centration in this assay. These results indicate that xylitol inhibits 1α,25(OH)2D3-induced osteoclastogenesis by reducing the sRANKL/OPG expression ratio in osteoblastic cells.
4,000원
