An article published this year in “Springer Link” using one of our products, “PE Mouse anti-Human CD31”, by our customers from Department of Pharmacology and Razi Drug Research Center, School of Medicine Iran, University of Medical Sciences Tehran, Iran, in the analysis of how 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. Congrats and Thanks.
Summay:
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.
Reference:
Product link:
PE Mouse anti-Human CD31
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