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      • Modifying Action of Chitosan Oligosaccharide on 2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx)-induced Mutagenesis

        Shon, Yun-Hee,Ha, Young-Min,Jeong, Teuk-Rae,Kim, Cheorl-Ho,Nam, Kyung-Soo Korean Society for Biochemistry and Molecular Biol 2001 Journal of biochemistry and molecular biology Vol.34 No.1

        The mutagenic activity of chitosan oligosaccharide and its antimutagenic effect against 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) were investigated using the Salmonella/Ames test. No mutagenic activity was found in the Salmonella typhimurium strains TA 98 and TA 100, either with or without S9 activation. In contrast, chitosan oligosaccharide showed an inhibitory effect on the mutagenic activity of the cooked food mutagen, MeIQx, in the presence of S9. The influence of chitosan oligosaccharide on the genotoxicity of MeIQx was examined using a host-mediated assay in mice. The oligosaccharide was administered for 14 consecutive days (intragastric application at doses of 0.1 or 0.5 g/kg body wt) to mice. S. typhimurium TA 98 was given intravenously before an oral dose of MeIQx (4.5 mg/kg body wt.). The number of $his^+$ revertants were determined from the Ever of mice. The intragastric application of oligosaccharide led to a 47% reduction in the number of mutants induced by MeIQx (p<0.05). These results suggested that chitosan oligosaccharide had antimutagenic properties against MeIQx in vitro and in vivo.

      • KCI등재

        Effects of N-Acetylglucosamine on Suppression of Collagenolysis and Bone Resorption in Mouse Calvarial Osteoblasts

        Park, Cheon,Chung, Kang Hyun,Jeong, Teuk Rae,Yang, Hyun Pill,Nam, Kyung Soo,Kim, Cheorl Ho 한국키틴키토산학회 2000 한국키틴키토산학회지 Vol.5 No.2

        생쥐의 osteoblasts를 골재흡수 약물인 PTH, 1,25(OH) 2D3, 그리고 IL-1으로 자극시키면 gelatinase생산을 촉진하여 콜라겐분해가 증가하지만, indomethacin과 dexamethasone은 생쥐의 osteoblastic세포의 collagenolysiss를 저해하였다. 골재흡수에 IL-1을 생쥐태아 유래의 장골조직 배양 (fetal mouse long bone organ culture)에 처리하자 IL-1 은 골재흡수를 촉진하였다. 이러한 골대사의 지견을 바탕으로 키린의 분해잔기인 N-acetylglucosamine의 활성을 검정하였다. 시험관내 독성검사에서 N-acetylglucosamine 1-200 yg/ml의 농도에서는 독성이 없었다. N-acetylglucosamine은 PTH (2units/ml), MCM (5%, v/v), IL-1α (1 ng/ml) 1,25(OH) 2D3 (10 ng/ml)처리에 대해서 그리고 IL-1α와 IL-1β-유발collagenolysis에 대해서도 보호효과를 나타내었다. N-acetylglucosamine을 1시간동안 전처리와 후처리에서 콜라겐분해에 약간의 보호활성이 있었으며 IL-1 α 와 IL-1 β 에 의해 유발되는 콜라겐분해에 보호활성이 보였다. 1시간동안 전처리는 콜라겐분해를 감소시키며, N-acetylglucosamine은 gelatinase효소를 저해하였으며 PTH,1,25(OH) 2D3, IL-1 β 및 IL-1 α로 유발된 효소활성화가 저해되었다. 즉, N-acetylglucosamine은 IL-1 α - and IL-1 β에 의해 촉진되는 골재흡수에 효과적이었으며. 이러한 결과는 N-acetylglucosamine가 골다공증치료에 효과적임을 나타내는 것이다. We show that mouse calvarial osteoblasts in culture constitutively synthesize progelatinase-A. Then, mouse osteoblasts, which were stimulated by PTH, 1,25(OH)2D3, mononuclear cell conditioned medium (MCM) and IL-1 as bone resorption agents, showed increased collagenolysis by producing the active gelatinase. However, treatment of indomethacin and dexamethasone significantly decreased those effects of collagenolysis in mouse osteoblastic cells. On the other hand, IL-1 in stimulating bone resorption was examined using fetal mouse long bone organ culture. IL-1 stimulated bone resorption and produced marked resorption when present simultaneously. Furthermore, when it was examined the effects of indomethacin and dexamethasone on the dose dependent responses of IL-1 α , indomethacin and dexametasone produced a rightward shift in the IL-1dose response curve. The results of in vitro cytotoxicities showed that N-acetylglucosamine have no any cytotoxicities in concentrations of 1-200 yg/ml and furthermore there is no any cytotoxicity even in concentration of 300 yg/ml on mouse calvarial bone cells. N-acetylglucosamine had Protective activity against PTH (2 units/ml), or MCM (5%, v/v), or IL-1 α (1 ng/ml) or 1,25(OH) 2D3 (10 ng/ml), IL-1 α and IL-1β-induced collagenolysis in the mouse calvarial cells. Pretreatment of theN-acetylglucosamine for 1 h, which by itself had little effect on cell survival, did not enhance the collagenolysis, nor significantly reduced the collagenolysis by pretreatment. Furthermore, the medicinal extracts were shown to have the protective effects against collagenolysis induced by IL-1 α and IL-1 β. Pretreatment of the extracts for 1 h significantly reduced the collagenolysis. Interestingly, the N-acetylglucosamine were shown to have the inhibiting effects against gelatinase enzyme and prosseing activity induced by the bone resortion agents of PTH, 1,25(OH)2D3, IL-1 β and IL-1 α , with strong protective effect in pretreatment with the extracts. JV-acetylglucosamine were shown to have the inhibiting effects against IL-1 α - and IL-1 β -stimulated bone resorption and the effect of the pretreatment with a various concentrations of the medicinal extracts were significant. The inhibition extent and phenomena of IL-1-stimulated bone resorption by nonsteroidal anti-inflammatory agents of indomethacin and dexamethasone were similar to those obtained by H-acetylglucosamine treatment in the mouse calvarial tissue culture system. These results indicated that the N-acetylglucosamine are highly stable and applicable to clinical uses in osteoporosis.

      • KCI등재
      • SCIESCOPUSKCI등재

        Modifying Action of Chitosan Oligosaccharide on 2 - Amino - 3,8 - dimethylimidazo[ 4,5 - f] quinoxaline(MeIQx) - induced Mutagenesis

        Kim, Cheorl Ho,Shon, Yun Hee,Nam, Kyung Soo,Ha, Young Min,Jeong, Teuk Rae 생화학분자생물학회 2002 BMB Reports Vol.34 No.1

        The mutagenic activity of chitosan oligosaccharide and its antimutagenic effect against 2-amino-3,8-dimethylimidazo [4,5-f]quinoxaline (MeIQx) were investigated using the Salmonella/Ames test. No mutagenic activity was found in the Salmonella typhimurium strains TA 98 and TA 100, either with or without S9 activation. In contrast, chitosan oligosaccharide showed an inhibitory effect on the mutagenic activity of the cooked food mutagen, MeIQx, in the presence of S9. The influence of chitosan oligosaccharide on the genotoxicity of MeIQa~ was examined using a hostmediated assay in mice. The oligosaccharide was administered for 14 consecutive days (intragastric application at doses of 0.1 or 0.5 g/㎏ body wt) to mice. S. typhimurium TA 98 was given intravenously before an oral dose of MeIQx (4.5 ㎎/㎏ body wt.). The number of his^+ revenants were determined from the Ever of mice. The intragastric application of oligosaccharide led to a 47% reduction in the number of mutants induced by MeIQx (p$lt;0.05). These results suggested that chitosan oligosaccharide had antimutagenic properties against MeIQx in vitro and in vivo.

      • KCI등재

        키토산 올리고당의 암예방 효과

        남미영,손윤희,김세권,정특래,남경수 한국키틴키토산학회 2000 한국키틴키토산학회지 Vol.5 No.2

        Chitosan Oligosaccharides (COS), COS I (M.W.: 3,000~5,000 daltons) and COS H (M.W. : 1,000~3,000daltons), were tested for their chernopreventive potentials using three biochemical markers of carcinogenesissuch as quinone reductase, glutathione S-transferase and glutathione. COS I and COS H were potent inducers of quinone reductase activity in murine hepatoma cells (Hepalclc7). Glutathione S-transferase activity was increased about 1.5 fold with COS Ⅱ in cultured murine hepatoma cells. In addition glutathione levels were slightly increased with COS Ⅰ. These results suggest that Chitosan Oligosaccharides has a chernopreuentive potential by inducing quinone reductase and glutathione S-transferase activities and increasing glutathione levels.

      • KCI등재

        엔아세칠글루코사민의 골대사보호활성

        박천(Cheon Park),박준호(Joon Ho Park),이문조(Moon Jo Lee),김동수(Dong Soo Kim),정특대(Teuk Rae Jeong),이경우(Kyeong Woo Lee),남경수(Kyung Soo Nam),김철호(Cheorl Ho Kim) 한국키틴키토산학회 2001 한국키틴키토산학회지 Vol.6 No.2

        IL-1β가 농도의존적으로 골세포에 영향을 주는지 해명하기 위하여 배양된 골아세포의 세포증식과 prostaglandin E2합성 그리고 plasminogen activator활성에 대한 영향을 검토한 결과 이들을 촉진하였다. 그러나 비타민D에 따라 반응하는 골아세포의 특징으로 알려진 osteocalcin생합성과 alkaine phosphatase활성의 유도생성은 IL-1β에 의해 오히려 길항적이었다. 이러한 결과는 골세포대사의 병리학적인 조절과정에서 IL-lβ가 골다공증의 병리학적 역할을 규명하는 새로운 결과이다. IL-1β에 의한 골흡수현상이 생리의 calvarial골세포에서 calcitonin처리로 크게 억제되어, 결과적으로 이러한 결과는IL-lβ에 의해 유발되는 골재흡수란 osteoclast에 의한다는 사실을 시사하였다. 한편, 키틴의 효소분해 단당잔기인 N-acetylslucosamine의 골대사에 미치는 활성을 검정하기 위하여 IL-1β-유발 PGE2생산에 대한 저해정도를 시험한 결과세포의 생존에는 크게 영향을 미치지 않고 PGE2합성만을 특이적으로 저해하였다. 또한, N-acetylglucosamine을 1시간 동안 여러 가지 농도로 전처리하고 다음으로 PGE2-유도시약을 처리한 결과, PGE2합성을 억제하였으며 동시에 IL-1β에 의해유도된 plasminogen 의존적인 fibrinolysis을 억제하는 보호효과가 인정되었다. 한편. calcitonin처리가 IL-1β-촉진 골재흡수에 대한 저해활성을 보였으며 이러한 결과들은 calcitonin과 N-acetylglucosamine이 osteoclast매개성 골재흡수의 억제에 핵심적인 역할을 함을 시사하며 골흡수치료제로서의 근거를 제시하였다고 사료된다. When the mouse calvarial bone cells were used, the bone resorption induced by IL-1β was strongly inhibited by calcitonin treatment, indicating osteoclast-mediated bone resorption. On the other hand, the medicinal extracts of N-acetylglucosamine was tested for whether they could inhibit IL-1β-induced PGE2 production. Cell viability was not significantly affected by treatment with the indicated concentration of the extracts. The N-acetylglucosamine was shown to have the inhibitory effects against the synthesis of PGE2. We also examined the effect of the pretreatment with a various concentrations of the N-acetylglucosamine then treated the PGE2-induction agents. Pretreatment of the N-acetylglucosamine for 1 h, which by itself had little effect on cell survival. did not enhance the synthesis of PGE2. Furthermore, the N-acetylglucosamine were shown to have the protective effects against plasminogen dependent fibrinolysis induced by the bone resorption agents of IL-1β. Pretreatment of the N-acetytglu-cosamine for 1 h did not enhance the plasminogen dependent fibrinolysis. Finally, calcitonin showed the inhibitory activity the IL-1β-stimulated bone resorption in the mouse calvarial bone cells having both of the osteoblast and osteoclast cells. Seemingly, pretreatment of the N-acetylglucosamine for 1 h reduced the bone resorption. These results clearly indicated that calcitonin and N-acetylglucosamine play key roles in inhibition of the osteoclast-mediated bone resorption.

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