Potential modulatory mechanisms of action by long-chain polyunsaturated fatty acids on bone cell and chondrocyte metabolism

Abshirini, Maryam; Ilesanmi-Oyelere, Bolaji Lilian; Kruger, Marlena C.

doi:10.1016/j.plipres.2021.101113

Cited by 70 publications

(52 citation statements)

References 83 publications

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“…Omega-3 fatty acids reduce oxidative stress and apoptosis via the NF-κB and the iNOS pathways. Dietary fatty acids may modulate osteogenic differentiation in mesenchymal stem cells by up-regulation in phosphorylation of protein kinase B (Akt) at the plasma membrane ( Wauquier et al, 2009 ; Abshirini et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

In Sickness and in Health: The Oxygen Reactive Species and the Bone

Reis

Ramos

2021

Front. Bioeng. Biotechnol.

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Oxidative stress plays a central role in physiological and pathological bone conditions. Its role in signalment and control of bone cell population differentiation, activity, and fate is increasingly recognized. The possibilities of its use and manipulation with therapeutic goals are virtually unending. However, how redox balance interplays with the response to mechanical stimuli is yet to be fully understood. The present work summarizes current knowledge on these aspects, in an integrative and broad introductory perspective.

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Section: Discussionmentioning

confidence: 99%

In Sickness and in Health: The Oxygen Reactive Species and the Bone

Reis

Ramos

2021

Front. Bioeng. Biotechnol.

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“…QCT exhibited a protective effect on bone homeostasis to a large extent despite negative results from a few studies [ 22 ]. Additionally, QCT regulated bone metabolism through the MAPK signaling pathway and facilitated osteoclast activation by regulating the RANKL (Receptor Activator of Nuclear Factor-κB Ligand)/RANK/OPG (Osteoprotegerin) signal pathway [ 23 ]. However, despite these advances, the pharmacological mechanism of QCT on anti-OP remains limited.…”

Section: Introductionmentioning

confidence: 99%

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Yuan

Cai

et al. 2022

Life

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Since osteoporosis critically influences the lives of patients with a high incidence, effective therapeutic treatments are important. Quercetin has been well recognized as a bone-sparing agent and thus the underlying mechanisms warrant further investigation. In the current study, the network pharmacology strategy and zebrafish model were utilized to explain the potential pharmacological effects of quercetin on osteoporosis. The potential targets and related signaling pathways were explored through overlapping target prediction, protein–protein interaction network construction, and functional enrichment analysis. Furthermore, we performed docking studies to verify the specific interactions between quercetin and crucial targets. Consequently, 55 targets were related to osteoporosis disease among the 159 targets of quercetin obtained by three database sources. Thirty hub targets were filtered through the cytoNCA plugin. Additionally, the Gene Ontology functions in the top 10 respective biological processes, molecular functions, and cell components as well as the top 20 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were depicted. The most significance difference in the KEGG pathways was the TNF signaling pathway, consisting of the Nuclear Factor Kappa B Subunit (NF-κB), Extracellular Regulated Protein Kinases (ERK) 1/2, Activator Protein 1 (AP-1), Interleukin 6 (IL6), Transcription factor AP-1 (Jun), and Phosphatidylinositol 3 Kinase (PI3K), which were probably involved in the pharmacological effects. Moreover, molecular docking studies revealed that the top three entries were Interleukin 1 Beta (IL1B), the Nuclear Factor NF-Kappa-B p65 Subunit (RelA), and the Nuclear Factor Kappa B Subunit 1 (NFKB1), respectively. Finally, these results were verified by alizarin red-stained mineralized bone in zebrafish and related qPCR experiments. The findings probably facilitate the mechanism elucidation related to quercetin anti-osteoporosis action.

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“…Previous studies reported that supplementation with these vitamins can prevent and improve OA because of their antioxidant and anti-inflammatory effects ( Heidari and Babaei, 2019 ; Fuggle et al, 2020 ). Arachidonic acid and its metabolite prostaglandin E2 are key modulators of osteoclast differentiation and play important roles in bone diseases including OA ( Abshirini et al, 2021 ). Therefore, MY may relieve OA by regulating the pathways of the intestinal immune network for IgA production, steroid hormone biosynthesis, vitamin digestion and absorption, and arachidonic acid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Miya Improves Osteoarthritis Characteristics via the Gut-Muscle-Joint Axis According to Multi-Omics Analyses

Yang

Liu

et al. 2022

Front. Pharmacol.

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Background: The gut microbiota is associated with osteoarthritis (OA) progression. Miya (MY) is a product made from Clostridium butyricum, a member of gut microbiota. This study was conducted to investigate the effects of MY on OA and its underlying mechanisms.Methods: An OA rat model was established, and MY was used to treat the rats for 4 weeks. Knee joint samples from the rats were stained with hematoxylin-eosin, and fecal samples from the OA and OA+MY groups were subjected to 16S rDNA sequencing and metabolomic analysis. The contents of succinate dehydrogenase and muscle glycogen in the tibia muscle were determined, and related genes and proteins were detected using quantitative reverse transcription polymerase chain reaction and western blotting.Results: Hematoxylin and eosin staining showed that treatment with MY alleviated the symptoms of OA. According to the sequencing results, MY significantly increased the Chao1, Shannon, and Pielou evenness values compared to those in the untreated group. At the genus level, the abundances of Prevotella, Ruminococcus, Desulfovibrio, Shigella, Helicobacter, and Streptococcus were higher in the OA group, whereas Lactobacillus, Oscillospira, Clostridium, and Coprococcus were enriched after MY treatment. Metabolomic analysis revealed 395 differentially expressed metabolites. Additionally, MY treatment significantly increased the succinate dehydrogenase and muscle glycogen contents in the muscle caused by OA (p > 0.05). Finally, AMPK, Tfam, Myod, Ldh, Chrna1, Chrnd, Rapsyn, and Agrin were significantly downregulated in the muscles of OA mice, whereas Lcad, Mcad, and IL-1β were upregulated; MY significantly reversed these trends induced by OA.Conclusions: MY may promote the repair of joint damage and protect against OA via the gut-muscle-joint axis.

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Potential modulatory mechanisms of action by long-chain polyunsaturated fatty acids on bone cell and chondrocyte metabolism

Cited by 70 publications

References 83 publications

In Sickness and in Health: The Oxygen Reactive Species and the Bone

In Sickness and in Health: The Oxygen Reactive Species and the Bone

Exploring Quercetin Anti-Osteoporosis Pharmacological Mechanisms with In Silico and In Vivo Models

Miya Improves Osteoarthritis Characteristics via the Gut-Muscle-Joint Axis According to Multi-Omics Analyses

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