Effects of cholic acid modified glucosamine on chondrogenic differentiation

Xue, Jingchen; Song, Wenjing; Hui-yuan, Yao; Hou, Sirun; Liu, Sa; Wang, Yingjun; Pei, Duanqing; Zhu, Jiale; Qin, Dajiang; Li, Ren

doi:10.1039/c6ra09547j

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…Glucosamine and its derivatives inhibit osteoclastic differentiation [120] and enhance stem cells proliferation [121][122][123][124], chondrogenic differentiation or chondrogenesis [106,[122][123][124][125][126][127] and osteoblastic differentiation [120]. Glucosamine (0.1 and 1 mM) and N-acetyl glucosamine induced differentiation of mouse MC3T3-E1 osteoblasts by increasing the mineralisation of extracellular matrix and the expression of osteopontin (middle-stage osteoblastic differentiation biomarker) and osteocalcin (late-stage osteoblastic differentiation biomarker) [120].…”

Section: Induction Of Tissue Regeneration Stem Cell Proliferation Amentioning

confidence: 99%

Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

et al. 2019

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Osteoarthritis (OA) is a joint disease resulting from cartilage degeneration and causing joint pain and stiffness. Glucosamine exerts chondroprotective effects and effectively reduces OA pain and stiffness. This review aims to summarise the mechanism of glucosamine in protecting joint health and preventing OA by conducting a literature search on original articles. Current evidence has revealed that glucosamine exhibits anti-inflammatory effects by reducing the levels of pro-inflammatory factors (such as tumour necrosis factor-alpha, interleukin-1, and interleukin-6) and enhancing the synthesis of proteoglycans that retard cartilage degradation and improve joint function. Additionally, glucosamine improves cellular redox status, reduces OA-mediated oxidative damages, scavenges free radicals, upregulates antioxidant proteins and enzyme levels, inhibits the production of reactive oxygen species, and induces autophagy to delay OA pathogenesis. In conclusion, glucosamine prevents OA and maintains joint health by reducing inflammation, improving the redox status, and inducing autophagy in joints. Further studies are warranted to determine the synergistic effect of glucosamine with other anti-inflammatory and/or antioxidative agents on joint health in humans.

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Section: Induction Of Tissue Regeneration Stem Cell Proliferation Amentioning

confidence: 99%

Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

et al. 2019

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“…Comparable in its therapeutic effects on cartilage are the actions of CA and other bile acid members. For instance, by controlling the changes in genes and proteins linked to cartilage, CAmodified glucosamine encourages the production of cartilage [8]. On the other hand, CA increased the frequency and intensity of inflammatory erosive arthritis in different research [9].…”

Section: Introductionmentioning

confidence: 99%

Cholic acid mitigates osteoarthritis by inhibiting the NF-κB/PERK/SIRT1 signaling pathway

SHENG,

YI,

et al. 2024

BIOCELL

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Introduction: Cholic acid (CA) is a natural steroid useful in treating chronic bronchitis and cholecystitis. On the other hand, its potential impact on osteoarthritis (OA) is unknown. Objective: Using an in vitro and in vivo osteoarthritis model, we sought to assess the chondroprotective properties of CA. Methods: We employed the Cell Counting Kit-8 to measure the impact of CA on chondrocyte activity to assess the toxicity of the cells. Multiple molecular biology experimental techniques were used to investigate potential signaling pathways that CA may use to prevent inflammation and give chondrocytes protection. Furthermore, how CA affects the OA model in Sprague-Dawley (SD) rats was evaluated. Results: CA significantly suppressed the up-regulation of the interleukin-1 β (IL-1β), cyclooxygenase-2 (COX-2), and matrix metalloproteinase 13 (MMP-13) and the downregulation of aggrecan and type II collagen A1 (COL2A) in chondrocytes treated tumor necrosis factor-alpha (TNF-α). Differentially expressed genes (DEG) enrichment revealed IL-17, TNF, chemokine, cytokine-cytokine receptor, toll-like receptor, and nucleotide oligomerization domain-like receptor were the primary signaling pathways. The enriched DEGs included CXCL6, CCL20, MMP3, CXCL3, CXCL11, CCL5, CXCL10, MMP9, MMP13, and CXCL2; these DEGs are involved in inflammatory responses and their expression induced by TNF-α was reversed by CA treatment. CA inhibits p65 nuclear translocation and inhibitory subunit kappa B alpha (IκBα) phosphorylation induced by TNF-α. Furthermore, CA attenuated protein expression of protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositolrequiring transmembrane kinase/endoribonuclease 1α (IRE1α), glucose regulatory protein 78 (GRP78), and sirtuin 1 (SIRT1), and down-regulation of phosphorylation of AMP-activated protein kinase-α (p-AMPKα) in TNF-α-treated chondrocytes. Conclusions: CA significantly ameliorated cartilage degradation in the OA rat model. CA alleviated the inflammatory response through the nuclear factor kappa B/PERK/SIRT1 axis and ameliorated cartilage degradation.

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A short review on the synthesis of pyrrolo[3,4-c]coumarins an isolamellarin-B scaffolds

Patra¹

2022

Synthetic Communications

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Effects of cholic acid modified glucosamine on chondrogenic differentiation

Abstract: Glucosamine hydrochloride is a widely used drug for the treatment of osteoarthritis and can be easily modified by other molecules because of its alterable functional groups.

Cited by 4 publications

References 27 publications

Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

Cholic acid mitigates osteoarthritis by inhibiting the NF-κB/PERK/SIRT1 signaling pathway

A short review on the synthesis of pyrrolo[3,4-c]coumarins an isolamellarin-B scaffolds

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