The mechanism of transglutaminase 2 inhibition with glucosamine: implications of a possible anti-inflammatory effect through transglutaminase inhibition

Jeong, Kyung‐Chae; Ahn, Kyung-Ohk; Lee, Byung Il; Lee, Chang‐Hoon; Kim, Soo-Youl

doi:10.1007/s00432-009-0645-x

Cited by 13 publications

(8 citation statements)

References 37 publications

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“…This suggests that one microbial mediated effect of butyrate produced from C fermentation is reduced translocation of LPS and subsequent expression of NF-κB-based inflammation mediators. Several in vitro studies have demonstrated reduced activation of NF-κB with G and/or C [45][46][47]. Further, we reported previously that C-reactive protein, a target of NF-κB regulation, was down regulated in response to G&C in an intervention study in healthy adults [8].…”

Section: Discussionmentioning

confidence: 68%

Modulation of Gut Microbiota by Glucosamine and Chondroitin in a Randomized, Double-Blind Pilot Trial in Humans

et al. 2019

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Glucosamine and chondroitin (G&C), typically taken for joint pain, are among the most frequently used specialty supplements by US adults. More recently, G&C have been associated with lower incidence of colorectal cancer in human observational studies and reduced severity of experimentally-induced ulcerative colitis in rodents. However, little is known about their effects on colon-related physiology. G&C are poorly absorbed and therefore metabolized by gut microbiota. G&C have been associated with changes in microbial structure, which may alter host response. We conducted a randomized, double-blind, placebo-controlled crossover trial in ten healthy adults to evaluate the effects of a common dose of G&C compared to placebo for 14 days on gut microbial community structure, measured by 16S rRNA gene sequencing. Linear mixed models were used to evaluate the effect of G&C compared to placebo on fecal microbial alpha and beta diversity, seven phyla, and 137 genera. Nine genera were significantly different between interventions (False Discovery Rate < 0.05). Abundances of four Lachnospiraceae genera, two Prevotellaceae genera, and Desulfovibrio were increased after G&C compared to placebo, while Bifidobacterium and a member of the Christensenellaceae family were decreased. Our results suggest that G&C affect the composition of the gut microbiome which may have implications for therapeutic efficacy.

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Section: Discussionmentioning

confidence: 68%

Modulation of Gut Microbiota by Glucosamine and Chondroitin in a Randomized, Double-Blind Pilot Trial in Humans

et al. 2019

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“…These results are consistent with the effect of GS in several cell lines such as macrophages and human chondrocytes (Largo et al ., 2003). GS inhibited significantly Tgase-2 at high concentrations (Kim et al ., 2009; Jeong et al ., 2010) and Tgase-2 activates NF-κB which is involved in TPA-induced ear edema models (Lee et al ., 2004; Rafi et al ., 2007). But, the role of Tgase-2 has not been studied in TPA-induced inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, glucosamine was reported to act as a chemo-sensitizer via inhibition of transglutaminase-2 (Tgase-2) in doxorubicin-resistant MCF7 cells (Kim et al ., 2009; Jeong et al ., 2010).…”

Section: Introductionmentioning

confidence: 99%

Suppression of Transglutaminase-2 is Involved in Anti-Inflammatory Actions of Glucosamine in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Skin Inflammation

Park¹,

Cho²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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Glucosamine (GS) is well known for the treatment of inflam-mation. However, the mechanism and efficacy of GS for skin inflammation are unclear. The aim of this study was to evaluate the effects and mechanism of GS in the mouse 12-O-tetradecanoyl 13-acetate (TPA)-induced ear edema model. TPA-induced ear edema was evoked in ICR or transglutaminase 2 (Tgase-2) (-/-) mice. GS was administered orally (10-100 mg/kg) or topically (0.5-2.0 w/v %) prior to TPA treatment. Orally administered GS at 10 mg/kg showed a 76 or 57% reduction in ear weight or myeloperoxidase, respectively, and a decreased expression of cyclooxy-genase-2 (COX-2), NF-κB and Tgase-2 in TPA-induced ear edema by western blot and immunohistochemistry. Role of Tgase-2 in TPA ear edema is examined using Tgase-2 (-/-) mice and TPA did not induce COX-2 expression in ear of Tgase-2 (-/-) mice. These observations suggested that Tgase-2 is involved in TPA-induced COX-2 expression in the inflamed ear of mice and anti-inflammatory effects of glucosamine is mediated through suppression of Tgase-2 in TPA ear edema.

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“…Several studies have demonstrated that NF-κB is a major regulatory factor in the pathogenesis of microglia-mediated neuroinflammation [ 21 , 22 ]. Many studies have suggested that gene expression of anti-inflammatory cytokines such as interleukin (IL)-10 [ 23 , 24 ] and pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, IL-1β, and monocyte chemotactic protein-1 (MCP-1) is controlled by the activation of NF-κB [ 25 , 26 , 27 , 28 , 29 , 30 , 31 ]. Among the anti-inflammatory cytokines, IL-10 has a variety of beneficial effects in the CNS.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Induces the Expression of Interleukin-10 and Brain-Derived Neurotrophic Factor in BV2 Microglia under Hypoxia

Song

Cheon

Jung

et al. 2014

IJMS

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Microglia are the resident macrophages of the central nervous system (CNS) and play an important role in neuronal recovery by scavenging damaged neurons. However, overactivation of microglia leads to neuronal death that is associated with CNS disorders. Therefore, regulation of microglial activation has been suggested to be an important target for treatment of CNS diseases. In the present study, we investigated the beneficial effect of resveratrol, a natural phenol with antioxidant effects, in the microglial cell line, BV2, in a model of hypoxia injury. Resveratrol suppressed the mRNA expression of the pro-inflammatory molecule, tumor necrosis factor-α, and promoted the mRNA expression of the anti-inflammatory molecule, interleukin-10, in BV2 microglia under hypoxic conditions. In addition, resveratrol inhibited the activation of the transcription factor, nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB), which is upstream in the control of inflammatory reactions in hypoxia-injured BV2 microglia. Moreover, resveratrol promoted the expression of brain-derived neurotrophic factor (BDNF) in BV2 microglia under hypoxic stress. Overall, resveratrol may promote the beneficial function of microglia in ischemic brain injury.

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The mechanism of transglutaminase 2 inhibition with glucosamine: implications of a possible anti-inflammatory effect through transglutaminase inhibition

Abstract: We concluded that GlcN inhibits TGase 2 activity by direct contact. GlcN and its metabolite GlcN6P can down-regulate constitutive activation of NF-κB in vivo via inhibition of TGase 2.

Cited by 13 publications

References 37 publications

Modulation of Gut Microbiota by Glucosamine and Chondroitin in a Randomized, Double-Blind Pilot Trial in Humans

Modulation of Gut Microbiota by Glucosamine and Chondroitin in a Randomized, Double-Blind Pilot Trial in Humans

Suppression of Transglutaminase-2 is Involved in Anti-Inflammatory Actions of Glucosamine in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Skin Inflammation

Resveratrol Induces the Expression of Interleukin-10 and Brain-Derived Neurotrophic Factor in BV2 Microglia under Hypoxia

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