Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes

Strategies based on mesenchymal stem cell (MSC) therapy for restoring injured articular cartilage are not effective enough in osteoarthritis (OA). Due to the enhanced inflammation and oxidative stress in OA microenvironment, differentiation of MSCs into chondrocytes would be impaired. This study aim...

Full description

Bibliographic Details
Main Authors: Bahrampour Juybari, Kobra, Kamarul, Tunku, Najafi, Mohammad, Jafari, Davood, Sharifi, Ali Mohammad
Format: Article
Published: Springer 2018
Subjects:
_version_ 1796961615499755520
author Bahrampour Juybari, Kobra
Kamarul, Tunku
Najafi, Mohammad
Jafari, Davood
Sharifi, Ali Mohammad
author_facet Bahrampour Juybari, Kobra
Kamarul, Tunku
Najafi, Mohammad
Jafari, Davood
Sharifi, Ali Mohammad
author_sort Bahrampour Juybari, Kobra
collection UM
description Strategies based on mesenchymal stem cell (MSC) therapy for restoring injured articular cartilage are not effective enough in osteoarthritis (OA). Due to the enhanced inflammation and oxidative stress in OA microenvironment, differentiation of MSCs into chondrocytes would be impaired. This study aims to explore the effects of diallyl disulfide (DADS) on IL-1β-mediated inflammation and oxidative stress in human adipose derived mesenchymal stem cells (hADSCs) during chondrogenesis. MTT assay was employed to examine the effects of various concentrations of DADS on the viability of hADSCs at different time scales to obtain non-cytotoxic concentration range of DADS. The effects of DADS on IL-1β-induced intracellular ROS generation and lipid peroxidation were evaluated in hADSCs. Western blotting was used to analyze the protein expression levels of IκBα (np), IκBα (p), NF-κB (np) and NF-κB (p). Furthermore, the gene expression levels of antioxidant enzymes in hADSCs and chondrogenic markers at days 7, 14 and 21 of differentiation were measured using qRT-PCR. The results showed that addition of DADS significantly enhanced the mRNA expression levels of antioxidant enzymes as well as reduced ROS elevation, lipid peroxidation, IκBα activation and NF-κB nuclear translocation in hADSCs treated with IL-1β. In addition, DADS could significantly increase the expression levels of IL-1β-induced impaired chondrogenic marker genes in differentiated hADSCs. Treatment with DADS may provide an effective approach to prevent the pro-inflammatory cytokines and oxidative stress as catabolic causes of chondrocyte cell death and enhance the protective anabolic effects by promoting chondrogenesis associated gene expressions in hADSCs exposed to OA condition.
first_indexed 2024-03-06T05:56:46Z
format Article
id um.eprints-22368
institution Universiti Malaya
last_indexed 2024-03-06T05:56:46Z
publishDate 2018
publisher Springer
record_format dspace
spelling um.eprints-223682019-09-17T01:28:37Z http://eprints.um.edu.my/22368/ Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes Bahrampour Juybari, Kobra Kamarul, Tunku Najafi, Mohammad Jafari, Davood Sharifi, Ali Mohammad R Medicine Strategies based on mesenchymal stem cell (MSC) therapy for restoring injured articular cartilage are not effective enough in osteoarthritis (OA). Due to the enhanced inflammation and oxidative stress in OA microenvironment, differentiation of MSCs into chondrocytes would be impaired. This study aims to explore the effects of diallyl disulfide (DADS) on IL-1β-mediated inflammation and oxidative stress in human adipose derived mesenchymal stem cells (hADSCs) during chondrogenesis. MTT assay was employed to examine the effects of various concentrations of DADS on the viability of hADSCs at different time scales to obtain non-cytotoxic concentration range of DADS. The effects of DADS on IL-1β-induced intracellular ROS generation and lipid peroxidation were evaluated in hADSCs. Western blotting was used to analyze the protein expression levels of IκBα (np), IκBα (p), NF-κB (np) and NF-κB (p). Furthermore, the gene expression levels of antioxidant enzymes in hADSCs and chondrogenic markers at days 7, 14 and 21 of differentiation were measured using qRT-PCR. The results showed that addition of DADS significantly enhanced the mRNA expression levels of antioxidant enzymes as well as reduced ROS elevation, lipid peroxidation, IκBα activation and NF-κB nuclear translocation in hADSCs treated with IL-1β. In addition, DADS could significantly increase the expression levels of IL-1β-induced impaired chondrogenic marker genes in differentiated hADSCs. Treatment with DADS may provide an effective approach to prevent the pro-inflammatory cytokines and oxidative stress as catabolic causes of chondrocyte cell death and enhance the protective anabolic effects by promoting chondrogenesis associated gene expressions in hADSCs exposed to OA condition. Springer 2018 Article PeerReviewed Bahrampour Juybari, Kobra and Kamarul, Tunku and Najafi, Mohammad and Jafari, Davood and Sharifi, Ali Mohammad (2018) Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes. Cell and Tissue Research, 373 (2). pp. 407-419. ISSN 0302-766X, DOI https://doi.org/10.1007/s00441-018-2825-y <https://doi.org/10.1007/s00441-018-2825-y>. https://doi.org/10.1007/s00441-018-2825-y doi:10.1007/s00441-018-2825-y
spellingShingle R Medicine
Bahrampour Juybari, Kobra
Kamarul, Tunku
Najafi, Mohammad
Jafari, Davood
Sharifi, Ali Mohammad
Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title_full Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title_fullStr Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title_full_unstemmed Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title_short Restoring the IL-1β/NF-κB-induced impaired chondrogenesis by diallyl disulfide in human adipose-derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
title_sort restoring the il 1β nf κb induced impaired chondrogenesis by diallyl disulfide in human adipose derived mesenchymal stem cells via attenuation of reactive oxygen species and elevation of antioxidant enzymes
topic R Medicine
work_keys_str_mv AT bahrampourjuybarikobra restoringtheil1bnfkbinducedimpairedchondrogenesisbydiallyldisulfideinhumanadiposederivedmesenchymalstemcellsviaattenuationofreactiveoxygenspeciesandelevationofantioxidantenzymes
AT kamarultunku restoringtheil1bnfkbinducedimpairedchondrogenesisbydiallyldisulfideinhumanadiposederivedmesenchymalstemcellsviaattenuationofreactiveoxygenspeciesandelevationofantioxidantenzymes
AT najafimohammad restoringtheil1bnfkbinducedimpairedchondrogenesisbydiallyldisulfideinhumanadiposederivedmesenchymalstemcellsviaattenuationofreactiveoxygenspeciesandelevationofantioxidantenzymes
AT jafaridavood restoringtheil1bnfkbinducedimpairedchondrogenesisbydiallyldisulfideinhumanadiposederivedmesenchymalstemcellsviaattenuationofreactiveoxygenspeciesandelevationofantioxidantenzymes
AT sharifialimohammad restoringtheil1bnfkbinducedimpairedchondrogenesisbydiallyldisulfideinhumanadiposederivedmesenchymalstemcellsviaattenuationofreactiveoxygenspeciesandelevationofantioxidantenzymes