Sodium butyrate abolishes the degradation of type II collagen in human chondrocytes

Wang, Bo; Zhou, Juan; Wang, Kunzheng

doi:10.1016/j.biopha.2018.03.062

Cited by 24 publications

(17 citation statements)

References 31 publications

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“…Butyrate could inhibit the production of key MMPs in chondrocytes via pro‐inflammatory cytokines at both mRNA and protein levels, which further potently inhibit cartilage collagen breakdown . Moreover, sodium butyrate markedly inhibits IL‐1β‐induced expression of MMPs and ADAMTSs by suppressing phosphorylation of IκBα, NF‐κB p65 and IKK to abolish inflammatory NF‐κB activation . Importantly, GPR43 receptor is greatly relevant to efficacy of butyrate in inhibiting IL‐1β‐induced inflammation in chondrocytes and its chemoattractant effects …”

Section: Modulation Of Fatty Acids On Specific Bone Cell Typesmentioning

confidence: 99%

“…257 Moreover, sodium butyrate markedly inhibits IL-1β-induced expression of MMPs and ADAMTSs by suppressing phosphorylation of IκBα, NF-κB p65 and IKK to abolish inflammatory NF-κB activation. 258 Importantly, GPR43 receptor is greatly relevant to efficacy of butyrate in inhibiting IL-1β-induced inflammation in chondrocytes and its chemoattractant effects. 259…”

Section: Fatty Acids and Chondrocytesmentioning

confidence: 99%

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Therapeutic potentials and modulatory mechanisms of fatty acids in bone

et al. 2019

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Bone metabolism is a lifelong process that includes bone formation and resorption. Osteoblasts and osteoclasts are the predominant cell types associated with bone metabolism, which is facilitated by other cells such as bone marrow mesenchymal stem cells (BMMSCs), osteocytes and chondrocytes. As an important component in our daily diet, fatty acids are mainly categorized as long‐chain fatty acids including polyunsaturated fatty acids (LCPUFAs), monounsaturated fatty acids (LCMUFAs), saturated fatty acids (LCSFAs), medium‐/short‐chain fatty acids (MCFAs/SCFAs) as well as their metabolites. Fatty acids are closely associated with bone metabolism and associated bone disorders. In this review, we summarized the important roles and potential therapeutic implications of fatty acids in multiple bone disorders, reviewed the diverse range of critical effects displayed by fatty acids on bone metabolism, and elucidated their modulatory roles and mechanisms on specific bone cell types. The evidence supporting close implications of fatty acids in bone metabolism and disorders suggests fatty acids as potential therapeutic and nutritional agents for the treatment and prevention of metabolic bone diseases.

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Section: Modulation Of Fatty Acids On Specific Bone Cell Typesmentioning

confidence: 99%

Section: Fatty Acids and Chondrocytesmentioning

confidence: 99%

Therapeutic potentials and modulatory mechanisms of fatty acids in bone

et al. 2019

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“…Interestingly, one study revealed that the anti-tumor properties of NaB were partly mediated by the activation of autophagy (Zhang et al, 2016), whereas another study reported that the restriction of mTOR complex 1 (mTORC1) by SCFAs could enhance the activation of autophagy (Noureldein and Eid, 2018). Furthermore, recent studies demonstrated that NaB could protect chondrocytes from interleukin (IL)-1β-induced inflammation and prevent the extracellular matrix (ECM) degradation of chondrocytes via the regulation of the nuclear factor-κB (NF-κB) pathway (Bo et al, 2018;Pirozzi et al, 2018), However, whether the protective effects of NaB on OA is partially mediated by the promotion of autophagy has not been wellinvestigated, and the exact mechanisms through which NaB enhances autophagy and its potential cartilage-protective effects in OA remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Microbial Metabolite Sodium Butyrate Attenuates Cartilage Degradation by Restoring Impaired Autophagy and Autophagic Flux in Osteoarthritis Development

Zhou

Wang

et al. 2021

Front. Pharmacol.

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Osteoarthritis (OA) is a degenerative joint disease with multiple etiologies that affects individuals worldwide. No effective interventions are currently available to reverse the pathological process of OA. Sodium butyrate (NaB), a component of short-chain fatty acids (SCFAs), has multiple biological activities, including the attenuation of inflammation and anti-tumor activities in various diseases. However, whether the protective effects of NaB in OA are associated with the promotion of autophagy had not been investigated. Here, we explored the chondroprotective properties of NaB in an interleukin (IL)-1β-induced inflammatory chondrocyte model and an anterior cruciate ligament transection (ACLT) mouse model. Hematoxylin and eosin (HE), Safranin O, and immunohistochemical staining were performed to evaluate the effects of NaB treatment on articular cartilage. An optimal NaB dose for chondrocyte treatment was determined via cell counting kit-8 assays. Immunofluorescence and transmission electron microscopy were used to detect autophagy in chondrocytes. Flow cytometry was utilized to detect reactive oxygen species (ROS), cell cycle activity, and apoptosis in chondrocytes. Western blot and immunostaining were performed to evaluate the protein expression levels of relevant indicators. We found that the administration of NaB by oral gavage could attenuate cartilage degradation. In parallel, NaB treatment could enhance the activation of autophagy, increase autophagic flux, decrease extracellular matrix degradation, and reduce apoptosis by restraining inflammation, ROS production, and cell cycle arrest in IL-1β-treated chondrocytes. The protective effects of NaB could be partially abolished by the autophagy inhibitor 3-methyladenine (3-MA), which indicated that the protective effects of NaB against OA were partially governed by the enhancement of autophagy to restrain the formation of inflammatory mediators and ROS and regulate cell cycle progression and apoptosis in chondrocytes. In conclusion, NaB could attenuate OA progression by restoring impaired autophagy and autophagic flux via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway, both in vitro and in vivo, implying that NaB could represent a novel therapeutic approach for OA.

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“…In addition, it is well known that SCFAs are involved in the activity of several types of immune cells, and it has been reported that SCFAs play important roles in the differentiation of Treg cells. Butyrate is known to determine the number and function of Treg cells in the intestine [13], and to prevent cartilage degradation by reducing type II collagen degradation [21]. L. rhamnosus is known to have an immunomodulatory effect through changes in the intestinal environment and various effectors, and to affect bone formation and chondrocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

Oral Administration of Lactobacillus Rhamnosus Ameliorates the Progression of Osteoarthritis by Inhibiting Joint Pain and Inflammation

Jhun¹,

Cho²,

Lee³

et al. 2021

Preprint

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Osteoarthritis (OA) is the most common form of arthritis and age-related degenerative joint disorder, which adversely affects quality of life and causes disability. However, the pathogenesis of OA remains unclear. This study was performed to examine the effects of Lactobacillus rhamnosus in OA progression. OA was induced in 6-week-old male Wistar rats by monosodium iodoacetate (MIA) injection, and the effects of oral administration of L. rhamnosus were examined in this OA rat model. Pain severity, cartilage destruction, and inflammation were measured in MIA-induced OA rats. The intestines were isolated from OA rats, and the intestinal structure and inflammation were measured. Protein expression in the dorsal root ganglion was analyzed by immunohistochemistry. The effects of L. rhamnosus on mRNA and protein expression in chondrocytes stimulated with interleukin (IL)-1β and lipopolysaccharide (LPS) were analyzed by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Pain severity was decreased in L. rhamnosus-treated MIA-induced OA rats. The levels of expression of MCP-1, a potential inflammatory cytokine, and its receptor, CCR2, were decreased, and GABA and PPAR-γ expression were increased in L. rhamnosus-treated OA rats. The inflammation, as determined by IL-1β, and cartilage destruction, as determined by MMP3, were also significantly decreased by L. rhamnosus in OA rats. Intestinal damage and inflammation were also improved by L. rhamnosus. In human OA chondrocytes, TIMP1, TIMP3, SOX9 and COL2A1 which are tissue inhibitors of MMP, and IL-10, an anti-inflammatory cytokine, were increased by L. rhamnosus.L. rhamnosus treatment led to decreased pain severity and cartilage destruction in a rat model of OA. Intestinal destruction and inflammation were also decreased by L. rhamnosus treatment. Our findings suggested the therapeutic potential of L. rhamnosus in OA.

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Sodium butyrate abolishes the degradation of type II collagen in human chondrocytes

Cited by 24 publications

References 31 publications

Therapeutic potentials and modulatory mechanisms of fatty acids in bone

Therapeutic potentials and modulatory mechanisms of fatty acids in bone

Microbial Metabolite Sodium Butyrate Attenuates Cartilage Degradation by Restoring Impaired Autophagy and Autophagic Flux in Osteoarthritis Development

Oral Administration of Lactobacillus Rhamnosus Ameliorates the Progression of Osteoarthritis by Inhibiting Joint Pain and Inflammation

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