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Amino Monosaccharide

The Experts below are selected from a list of 147 Experts worldwide ranked by ideXlab platform

Isao Nagaoka – 1st expert on this subject based on the ideXlab platform

  • Glucosamine suppresses interleukin-8 production and ICAM-1 expression by TNF-α-stimulated human colonic epithelial HT-29 cells
    International Journal of Molecular Medicine, 2020
    Co-Authors: Shin Yomogida, Koji Sakamoto, Isao Nagaoka

    Abstract:

    : Intestinal epithelial cells play an important role in the mucosal immune reaction in inflammatory bowel diseases via the production and expression of chemokines and adhesion molecules, such as interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1), which are involved in the neutrophil infiltration and tissue damage in the inflamed colon. Notably, glucosamine, a naturally-occurring Amino Monosaccharide, has been shown to exhibit an anti-inflammatory action by inhibiting neutrophil functions. In the present study, to evaluate the anti-inflammatory action of glucosamine on intestinal epithelial cells, we examined the effects of glucosamine on the activation of a human colonic epithelial cell line HT-29. The results revealed that glucosamine suppressed the IL-8 production and ICAM-1 expression by TNF-alpha-activated HT-29 cells. Furthermore, glucosamine inhibited the TNF-alpha-induced phosphorylation of p38MAPK and NF-kappaB p65, and the nuclear translocation of NF-kappaB in the cells. Thus, glucosamine demonstrates inhibitory actions on the inflammatory and signaling molecules (IL-8, ICAM-1, p38MAPK and NF-kappaB) in intestinal epithelial cells. However, glucosamine did not essentially affect the binding of TNF-alpha to its receptor on HT-29 cells. Together, these observations suggest that glucosamine may have the potential to exhibit an anti-inflammatory action on intestinal epithelial cells, by possibly interfering with the activation signaling downstream of the ligand/receptor binding.

  • Inhibitory actions of glucosamine on neutrophil functions
    Ensho Saisei, 2020
    Co-Authors: Isao Nagaoka, Shiori Suguro, Koji Sakamoto

    Abstract:

    Glucosamine, an Amino Monosaccharide occurring naturally in the connective and cartilage tissues, contributes to maintain the strength, flexibility and elasticity of these tissues. In recent years, glucosamine has been widely used to treat osteoarthritis in humans. Neutrophils, which usually function as the primary defenders in acute bacterial infections, are also implicated in the destructive inflammatory responses in arthritis. Recently, we have revealed the inhibitory actions of glucosamine on neutrophil functions. Glucosamine suppressed superoxide generation by neutrophils, and inhibited phagocytosis of opsonized particles. Furthermore, glucosamine inhibited the release of granule enzyme from phagocytosing neutrophils, and repressed chemotaxis. In addition, glucosamine significantly inhibited the upregulation of adhesion molecule CD 11 b, polymerization of actin and phosphorylation of p 38 MAPK, associated with neutrophil activation. Together these observations likely suggest that glucosamine suppresses the neutrophil functions, thereby exhibiting the anti-inflammatory actions in arthritis.

  • Recent aspects of the anti-inflammatory actions of glucosamine
    Carbohydrate Polymers, 2011
    Co-Authors: Isao Nagaoka, Shin Yomogida, Mamoru Igarashi, Y. Ju, Koji Sakamoto

    Abstract:

    Glucosamine, a naturally occurring Amino Monosaccharide, is present in the connective and cartilage tissues as a component of glycosAminoglycans. Thus, glucosamine has been widely used to treat osteoarthritis, a joint disease characterized by cartilage degeneration, in humans. In addition, glucosamine is expected to exert an anti-inflammatory action, since glucosamine suppresses inflammatory cell activation. To further extend the anti-inflammatory actions of glucosamine, we investigated the effects of glucosamine on synovial cells, endothelial cells and intestinal epithelial cells using in vitro and in vivo systems. Firstly, glucosamine suppressed the IL-1β-induced activation of synovial cells in vitro. Furthermore, glucosamine administration repressed synovial cell hyperplasia, cartilage destruction and inflammatory cell infiltration in rat adjuvant arthritis. Secondary, glucosamine suppressed the TNF-α-induced activation of intestinal epithelial cell HT-29 in vitro. In addition, glucosamine administration improved the clinical symptoms, and colonic inflammation and tissue injury in dextran sulfate sodium-induced colitis in rats. Finally, glucosamine suppressed the TNF-α-induced activation of endothelial cells in vitro. Moreover, glucosamine administration repressed the formation of atherosclerotic lesion and infiltration of inflammatory cells into the lesion in spontaneously hyperlipidemic mice B6 KOR Aposhl. Together these observations support the idea that glucosamine can function as not only a chondroprotective agent but also an anti-inflammatory molecule in the body.

Koji Sakamoto – 2nd expert on this subject based on the ideXlab platform

  • Glucosamine suppresses interleukin-8 production and ICAM-1 expression by TNF-α-stimulated human colonic epithelial HT-29 cells
    International Journal of Molecular Medicine, 2020
    Co-Authors: Shin Yomogida, Koji Sakamoto, Isao Nagaoka

    Abstract:

    : Intestinal epithelial cells play an important role in the mucosal immune reaction in inflammatory bowel diseases via the production and expression of chemokines and adhesion molecules, such as interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1), which are involved in the neutrophil infiltration and tissue damage in the inflamed colon. Notably, glucosamine, a naturally-occurring Amino Monosaccharide, has been shown to exhibit an anti-inflammatory action by inhibiting neutrophil functions. In the present study, to evaluate the anti-inflammatory action of glucosamine on intestinal epithelial cells, we examined the effects of glucosamine on the activation of a human colonic epithelial cell line HT-29. The results revealed that glucosamine suppressed the IL-8 production and ICAM-1 expression by TNF-alpha-activated HT-29 cells. Furthermore, glucosamine inhibited the TNF-alpha-induced phosphorylation of p38MAPK and NF-kappaB p65, and the nuclear translocation of NF-kappaB in the cells. Thus, glucosamine demonstrates inhibitory actions on the inflammatory and signaling molecules (IL-8, ICAM-1, p38MAPK and NF-kappaB) in intestinal epithelial cells. However, glucosamine did not essentially affect the binding of TNF-alpha to its receptor on HT-29 cells. Together, these observations suggest that glucosamine may have the potential to exhibit an anti-inflammatory action on intestinal epithelial cells, by possibly interfering with the activation signaling downstream of the ligand/receptor binding.

  • Inhibitory actions of glucosamine on neutrophil functions
    Ensho Saisei, 2020
    Co-Authors: Isao Nagaoka, Shiori Suguro, Koji Sakamoto

    Abstract:

    Glucosamine, an Amino Monosaccharide occurring naturally in the connective and cartilage tissues, contributes to maintain the strength, flexibility and elasticity of these tissues. In recent years, glucosamine has been widely used to treat osteoarthritis in humans. Neutrophils, which usually function as the primary defenders in acute bacterial infections, are also implicated in the destructive inflammatory responses in arthritis. Recently, we have revealed the inhibitory actions of glucosamine on neutrophil functions. Glucosamine suppressed superoxide generation by neutrophils, and inhibited phagocytosis of opsonized particles. Furthermore, glucosamine inhibited the release of granule enzyme from phagocytosing neutrophils, and repressed chemotaxis. In addition, glucosamine significantly inhibited the upregulation of adhesion molecule CD 11 b, polymerization of actin and phosphorylation of p 38 MAPK, associated with neutrophil activation. Together these observations likely suggest that glucosamine suppresses the neutrophil functions, thereby exhibiting the anti-inflammatory actions in arthritis.

  • Recent aspects of the anti-inflammatory actions of glucosamine
    Carbohydrate Polymers, 2011
    Co-Authors: Isao Nagaoka, Shin Yomogida, Mamoru Igarashi, Y. Ju, Koji Sakamoto

    Abstract:

    Glucosamine, a naturally occurring Amino Monosaccharide, is present in the connective and cartilage tissues as a component of glycosAminoglycans. Thus, glucosamine has been widely used to treat osteoarthritis, a joint disease characterized by cartilage degeneration, in humans. In addition, glucosamine is expected to exert an anti-inflammatory action, since glucosamine suppresses inflammatory cell activation. To further extend the anti-inflammatory actions of glucosamine, we investigated the effects of glucosamine on synovial cells, endothelial cells and intestinal epithelial cells using in vitro and in vivo systems. Firstly, glucosamine suppressed the IL-1β-induced activation of synovial cells in vitro. Furthermore, glucosamine administration repressed synovial cell hyperplasia, cartilage destruction and inflammatory cell infiltration in rat adjuvant arthritis. Secondary, glucosamine suppressed the TNF-α-induced activation of intestinal epithelial cell HT-29 in vitro. In addition, glucosamine administration improved the clinical symptoms, and colonic inflammation and tissue injury in dextran sulfate sodium-induced colitis in rats. Finally, glucosamine suppressed the TNF-α-induced activation of endothelial cells in vitro. Moreover, glucosamine administration repressed the formation of atherosclerotic lesion and infiltration of inflammatory cells into the lesion in spontaneously hyperlipidemic mice B6 KOR Aposhl. Together these observations support the idea that glucosamine can function as not only a chondroprotective agent but also an anti-inflammatory molecule in the body.

Yinghua Ju – 3rd expert on this subject based on the ideXlab platform

  • glucosamine a naturally occurring Amino Monosaccharide inhibits a549 and h446 cell proliferation by blocking g1 s transition
    Molecular Medicine Reports, 2013
    Co-Authors: Yinghua Ju, Aiming Yu, Didi Wu, Hongkai Zhang

    Abstract:

    : Uncontrolled proliferation is important in tumorigenesis. In the present study, the effects of glucosamine on lung cancer cell proliferation were investigated. The expression of cyclin E, one of the key cyclins in the G1/S transition, and Skp2, the ubiquitin ligase subunit that targets the negative cell cycle regulator, p27Kip1, were also assessed. Moreover, the underlying mechanisms of action of glucosamine were investigated in lung cancer cells. A549 and H446 cells were synchronized using thymidine in the presence or absence of glucosamine. The effect of glucosamine on lung cancer cell proliferation was determined by MTT assay. Cyclin E and p27Kip1 proteins and their phosphorylation levels were detected by western blot analysis. Furthermore, the effect of glucosamine on the cell cycle was evaluated by flow cytometry. Glucosamine was found to inhibit lung cancer cell proliferation and to suppress Skp2 and cyclin E expression. Notably, the phosphorylation levels of cyclin E (Thr62) and p27Kip1 (Thr187) were downregulated by glucosamine, and negatively correlated with degradation. Glucosamine was also found to arrest lung cancer cells in the G1/S phase. Thus, glucosamine may inhibit lung cancer cell proliferation by blocking G1/S transition through the inhibition of cyclin E and Skp2 protein expression.

  • Glucosamine, a naturally occurring Amino Monosaccharide, inhibits A549 and H446 cell proliferation by blocking G1/S transition
    Molecular Medicine Reports, 2013
    Co-Authors: Yinghua Ju, Aiming Yu, Didi Wu, Hongkai Zhang

    Abstract:

    : Uncontrolled proliferation is important in tumorigenesis. In the present study, the effects of glucosamine on lung cancer cell proliferation were investigated. The expression of cyclin E, one of the key cyclins in the G1/S transition, and Skp2, the ubiquitin ligase subunit that targets the negative cell cycle regulator, p27Kip1, were also assessed. Moreover, the underlying mechanisms of action of glucosamine were investigated in lung cancer cells. A549 and H446 cells were synchronized using thymidine in the presence or absence of glucosamine. The effect of glucosamine on lung cancer cell proliferation was determined by MTT assay. Cyclin E and p27Kip1 proteins and their phosphorylation levels were detected by western blot analysis. Furthermore, the effect of glucosamine on the cell cycle was evaluated by flow cytometry. Glucosamine was found to inhibit lung cancer cell proliferation and to suppress Skp2 and cyclin E expression. Notably, the phosphorylation levels of cyclin E (Thr62) and p27Kip1 (Thr187) were downregulated by glucosamine, and negatively correlated with degradation. Glucosamine was also found to arrest lung cancer cells in the G1/S phase. Thus, glucosamine may inhibit lung cancer cell proliferation by blocking G1/S transition through the inhibition of cyclin E and Skp2 protein expression.

  • glucosamine a naturally occurring Amino Monosaccharide modulates ll 37 induced endothelial cell activation
    International Journal of Molecular Medicine, 1998
    Co-Authors: Yinghua Ju, Koji Sakamoto, Hideoki Ogawa, Isao Nagaoka

    Abstract:

    Atheroscleros is now considered as a chronic inflammatory disease, and glucosamine has a potential to exhibit anti-inflammatory action. Thus, we investigated the effect of glucosamine on LL-37-induced endothelial cell activation. HUVEC (human umbilical vein endothelial cells) were stimulated by LL-37 in the presence or absence of glucosamine (0.01-1 mM) or its analogue, N-acetylglucosamine (0.1-1 mM). mRNA expression of MCP-1 (monocyte chemoattractant protein- 1) and ICAM-1 (intercellular adhesion molecule-1) was evaluated by real-time RT-PCR, and their protein levels were analyzed by ELISA and Western blotting, respectively. Furthermore, the effect of glucosamine on O -N-acetylglucosamine (O-G1cNAc) modification was evaluated by Western blotting. Glucosamine but not N-acetylglucosamine suppressed the LL-37-induced expression of MCP-1 and ICAM-1 at both mRNA (p<0.05 at 0.1 mM) and protein levels (p<0.05 at 1 mM). Of interest, O-G1cNAc modification was induced by incubating HUVEC with glucosamine (p<0.05 at 1 mM) but not N-acetylglucosamine. Of note, alloxan, an O -N-acetylglucosamine transferase inhibitor, which prevented the glucosamine-induced O-G1cNAc modification, abrogated the suppressive effect of glucosamine on MCP-1 and ICAM-1 expression (p<0.05 at 0.5 mM). These observations suggest that glucosamine modulates endothelial cell activation possibly via O-G1cNAc modification, and may exhibit an anti-inflammatory action on atherosclerosis.