Amino Monosaccharide

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Isao Nagaoka - One of the best experts 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.

  • Inhibitory action of glucosamine on platelet activation in guinea pigs
    Inflammation Research, 2005
    Co-Authors: J. F. Lu-suguro, Koji Sakamoto, Isao Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide, has been used to treat or prevent osteoarthritis in humans. Recently, we have revealed that glucosamine inhibits platelet activation in vitro . However, the effect of in vivo administration of glucosamine has not yet been clarified. In this study, we administered glucosamine orally to guinea pigs and examined its effects on platelet functions. Materials and methods: Glucosamine hydrochloride solution (0.5%, 5 mg/ml) was administered orally to guinea pigs ad libitum for 22 days, and platelet rich plasma was collected to evaluate platelet functions in vitro . Guinea pigs received an average of 400 mg glucosamine/animal/day. Results: Glucosamine-administration suppressed platelet aggregation in response to ADP by 51% ( p  

  • Inhibitory action of glucosamine on platelet activation in guinea pigs.
    Inflammation Research, 2005
    Co-Authors: J. F. Lu-suguro, Koji Sakamoto, Isao Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide, has been used to treat or prevent osteoarthritis in humans. Recently, we have revealed that glucosamine inhibits platelet activation in vitro. However, the effect of in vivo administration of glucosamine has not yet been clarified. In this study, we administered glucosamine orally to guinea pigs and examined its effects on platelet functions.

Koji Sakamoto - One of the best experts 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.

  • Inhibitory action of glucosamine on platelet activation in guinea pigs
    Inflammation Research, 2005
    Co-Authors: J. F. Lu-suguro, Koji Sakamoto, Isao Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide, has been used to treat or prevent osteoarthritis in humans. Recently, we have revealed that glucosamine inhibits platelet activation in vitro . However, the effect of in vivo administration of glucosamine has not yet been clarified. In this study, we administered glucosamine orally to guinea pigs and examined its effects on platelet functions. Materials and methods: Glucosamine hydrochloride solution (0.5%, 5 mg/ml) was administered orally to guinea pigs ad libitum for 22 days, and platelet rich plasma was collected to evaluate platelet functions in vitro . Guinea pigs received an average of 400 mg glucosamine/animal/day. Results: Glucosamine-administration suppressed platelet aggregation in response to ADP by 51% ( p  

  • Inhibitory action of glucosamine on platelet activation in guinea pigs.
    Inflammation Research, 2005
    Co-Authors: J. F. Lu-suguro, Koji Sakamoto, Isao Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide, has been used to treat or prevent osteoarthritis in humans. Recently, we have revealed that glucosamine inhibits platelet activation in vitro. However, the effect of in vivo administration of glucosamine has not yet been clarified. In this study, we administered glucosamine orally to guinea pigs and examined its effects on platelet functions.

Yinghua Ju - One of the best experts 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.

  • 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

  • modulation of tnf α induced endothelial cell activation by glucosamine a naturally occurring Amino Monosaccharide
    International Journal of Molecular Medicine, 1998
    Co-Authors: Yinghua Ju, Koji Sakamoto, Hideoki Ogawa, Isao Nagaoka
    Abstract:

    : Atherosclerosis is now considered a chronic inflammatory disease, and glucosamine has the potential to exhibit an anti-inflammatory action. Thus, we investigated the effect of glucosamine on tumor necrosis factor alpha (TNF-alpha)-induced endothelial cell activation. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNF-alpha in the presence or absence of glucosamine or its analogue, N-acetylglucosamine. mRNA expression of MCP-1 (a chemoattractant protein) and ICAM-1 (an adhesion molecule) was evaluated by real-time RT-PCR, and their protein levels were analyzed by ELISA and Western blotting, respectively. Furthermore, the effects of glucosamine on the phosphorylation of p38MAPK and NF-kappaB, and O-N-acetylglucosamine (O-GlcNAc) modification were evaluated by Western blotting. The results demonstrated that glucosamine but not N-acetylglucosamine suppressed TNF-alpha-induced expression of MCP-1 and ICAM-1 at both the mRNA and protein levels. Furthermore, glucosamine abrogated the phosphorylation of p38MAPK and NF-kappaB. To note, glucosamine induced O-GlcNAc modification, which was negatively correlated with the expression of MCP-1 and ICAM-1, and phosphorylation of p38MAPK and NF-kappaB. Thus, glucosamine is likely to suppress endothelial cell activation (TNF-alpha-induced ICAM-1 and MCP-1 expression) possibly by affecting p38MAPK and NF-kappaB signaling via O-GlcNAc modification.

Petya Dimitrova - One of the best experts on this subject based on the ideXlab platform.

  • Bone resorption and remodeling in murine collagenase-induced osteoarthritis after administration of glucosamine.
    Arthritis Research & Therapy, 2011
    Co-Authors: Nina Ivanovska, Petya Dimitrova
    Abstract:

    Introduction Glucosamine is an Amino-Monosaccharide and precursor of glycosAminoglycans, major components of joint cartilage. Glucosamine has been clinically introduced for the treatment of osteoarthritis but the data about its protective role in disease are insufficient. The goal of this study was to investigate the effect of long term administration of glucosamine on bone resorption and remodeling.

  • Bone resorption and remodeling in murine collagenase-induced osteoarthritis after administration of glucosamine
    Arthritis Research & Therapy, 2011
    Co-Authors: Nina Ivanovska, Petya Dimitrova
    Abstract:

    Introduction Glucosamine is an Amino-Monosaccharide and precursor of glycosAminoglycans, major components of joint cartilage. Glucosamine has been clinically introduced for the treatment of osteoarthritis but the data about its protective role in disease are insufficient. The goal of this study was to investigate the effect of long term administration of glucosamine on bone resorption and remodeling. Methods The effect of glucosamine on bone resorption and remodeling was studied in a model of collagenase-induced osteoarthritis (CIOA). The levels of macrophage-inflammatory protein (MIP)-1α, protein regulated upon activation, normal T-cell expressed, and secreted (RANTES), soluble receptor activator of nuclear factor kappa-B ligand (RANKL), tumor necrosis factor (TNF)-α, and interleukin (IL)-6, 4 and 10 in synovial fluid were measured by enzyme-linked immunosorbent assay (ELISA). Cell populations in synovial extracts and the expression of RANKL, of receptors for TNF-α (TNF-αR) and interferon γ (IFN-γR) on clusters of differentiation (CD) three positive T cells were analyzed by flow cytometry. Transforming growth factor (TGF)-β3, bone morphogenetic protein (BMP)-2, phosphorylated protein mothers against decapentaplegic homolog 2 (pSMAD-2), RANKL and Dickkopf-1 protein (DKK-1) positive staining in CIOA joints were determined by immunohistochemistry. Results The administration of glucosamine hydrochloride in CIOA mice inhibited loss of glycosAminoglycans (GAGs) and proteoglycans (PGs) in cartilage, bone erosion and osteophyte formation. It decreased the levels of soluble RANKL and IL-6 and induced IL-10 increase in the CIOA joint fluids. Glucosamine limited the number of CD11b positive Ly6G neutrophils and RANKL positive CD3 T cells in the joint extracts. It suppressed bone resorption via down-regulation of RANKL expression and affected bone remodeling in CIOA by decreasing BMP-2, TGF-β3 and pSMAD-2 expression and up-regulating DKK-1 joint levels. Conclusions Our data suggest that glucosamine hydrochloride inhibits bone resorption through down-regulation of RANKL expression in the joints, via reduction of the number of RANKL positive CD3 T cells and the level of sRANKL in the joints extracts. These effects of glucosamine appear to be critical for the progression of CIOA and result in limited bone remodeling of the joints.

S Suguro - One of the best experts on this subject based on the ideXlab platform.

  • Preventive actions of a high dose of glucosamine on adjuvant arthritis in rats.
    Inflammation Research, 2005
    Co-Authors: S Suguro, Koji Sakamoto, S. Hirano, Isao Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide has been used to treat or prevent osteoarthritis in humans. In this study, we evaluated the effect of glucosamine on rat adjuvant arthritis, a model of rheumatoid arthritis.

  • Preventive actions of a high dose of glucosamine on adjuvant arthritis in rats
    Inflammation Research, 2005
    Co-Authors: S Suguro, S. Hirano, K. Sakamoto, I. Nagaoka
    Abstract:

    Objective: Glucosamine, a naturally occurring Amino Monosaccharide has been used to treat or prevent osteoarthritis in humans. In this study, we evaluated the effect of glucosamine on rat adjuvant arthritis, a model of rheumatoid arthritis. Materials and methods: Adjuvant arthritis was induced in male Wistar rats by injection of Freund’s complete adjuvant (FCA) into the right hind paw, and 300 mg/kg of glucosamine, an extra-dose compared with a regular dose for osteoarthritis patients (1.5 g/day, approximately 25 mg/kg), was orally administered once a day to the arthritic rats for 22 days. Results: Glucosamine significantly suppressed the increase in arthritis score ( p < 0.05) after day 10 of adjuvant injection, and inhibited the swelling of FCA-injected right and -uninjected left hind paws ( p < 0.01) after day 18. In addition, histopathological examination of the arthritic joints revealed that glucosamine suppressed synovial hyperplasia, cartilage destruction and inflammatory cell infiltration. Furthermore, glucosamine reduced the production of nitric oxide and prostaglandin E_2 in plasma ( p < 0.05). Conclusions: These observations suggest that glucosamine is able to suppress the progression of adjuvant arthritis in rats. Glucosamine may be expected as a novel anti-inflammatory agent for treatment of rheumatoid arthritis.

  • glucosamine a naturally occurring Amino Monosaccharide suppresses the adp mediated platelet activation in humans
    Inflammation Research, 2004
    Co-Authors: S Suguro, Kazuhisa Iwabuchi, Yuko Tsutsumiishii, Koji Sakamoto, Isao Nagaoka
    Abstract:

    Objective: To evaluate the anti-thrombotic action of glucosamine, a naturally occurring Amino Monosaccharide, platelets were stimulated with ADP in the presence of glucosamine, and its effects on platelet functions were examined.

  • Glucosamine, a naturally occurring Amino Monosaccharide, suppresses the ADP-mediated platelet activation in humans
    Inflammation Research, 2004
    Co-Authors: S Suguro, Kazuhisa Iwabuchi, Koji Sakamoto, Y. Tsutsumi-ishii, Isao Nagaoka
    Abstract:

    Objective: To evaluate the anti-thrombotic action of glucosamine, a naturally occurring Amino Monosaccharide, platelets were stimulated with ADP in the presence of glucosamine, and its effects on platelet functions were examined. Materials and Methods: Human platelet-rich plasma was stimulated with 2.5 μM ADP in the presence of glucosamine (0.01 ~ 1 mM) or other Aminosugars (N-acetyl-glucosamine, galactosamine or N-acetyl-galactosamine, 1 mM), and platelet aggregation was monitored. Furthermore, the effects of glucosamine on the thromboxane A2 production, release of granule contents, intracellular calcium mobilization and phosphorylation of Syk (a 72 kD protein tyrosine kinase) were evaluated following ADP-stimulation. In addition, the binding of [^3H] ADP to its receptors was examined. Results: Glucosamine (>0.01 mM) dose-dependently suppressed platelet aggregation in response to ADP ( p < 0.05), whereas N-acetyl-glucosamine, galactosamine or N-acetyl-galactosamine (1 mM) did not affect the ADP-induced platelet aggregation. Furthermore, glucosamine (>0.1 mM) inhibited the extracellular release of granule contents (ATP and platelet factor 4) and production of thromboxane A_2 from ADP-stimulated platelets ( p < 0.05). Moreover, glucosamine significantly repressed the intracellular calcium mobilization at >0.1 mM and phosphorylation of Syk at >0.01 mM upon ADP-stimulation ( p < 0.05). In addition, glucosamine (>0.1 mM) inhibited the binding of ADP to its receptors ( p < 0.05). Conclusion: Glucosamine is able to suppress platelet aggregation, release of granule constituents, thromboxane A_2 production, calcium mobilization and phosphorylation of Syk possibly via the inhibition of ADP-binding to the receptors. Glucosamine could be expected as a novel anti-platelet agent for thrombotic disorders due to its suppressive actions on platelets.