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Abstract
Membrane-free stem cell components (MFSCC) from basal adipose tissue-derived stem cells (ADSCs) are unknown for the treatment strategies in osteoarthritis (OA). OA has been considered to be associated with inflammatory damage and cartilage degradation. In this study, we intended to investigate the molecular mechanism of the anti-inflammation and cartilage protection effect of MFSCC in vitro (rat primary chondrocytes) and in vivo (rat OA model). The MFSCC treatment significantly inhibited interleukin-1α (IL-1α) stimulated inflammation and cartilage degradation. The MFSCC considerably reduced the levels of inflammatory factors such as iNOS, COX-2, NO, and PGE2 and was suppressed NF-κB and MAPKs signaling pathways in IL-1α-stimulated rat chondrocytes. Additionally, biomarkers of OA such as MMP-9, COMP, and CTX-II decreased in the monosodium iodoacetate (MIA)-induced rat OA model by MFSCC treatment. In conclusion, the MFSCC was established to suppress IL-1α induced inflammation and cartilage degradation in vitro and in vivo. These findings provide new insight for understanding OA therapy using membrane-free stem cell approaches.
Highlights
Osteoarthritis (OA), an immensely prevalent cartilage degenerative disorder causing pain and functional impairment, represents an enormous societal and economic burden in the world [1]
We investigated whether the novel components of membrane-free stem cell components (MFSCC) from adipose tissue-derived stem cells (ADSCs) have an effect on anti-inflammation and cartilage regeneration in IL-1α-stimulated rat primary chondrocytes and a rat model of OA
The results suggest that MFSCC decreased the expression of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 in IL-1α-stimulated primary rat chondrocytes
Summary
Osteoarthritis (OA), an immensely prevalent cartilage degenerative disorder causing pain and functional impairment, represents an enormous societal and economic burden in the world [1]. OA is a well-established disease that affects all joint tissues, illustrated by the gradual degeneration of the articular cartilage, subchondral bone remodeling, vascular invasion of the articular surface, and synovial inflammation (synovitis) [2]. OA, being an age-related disease, affects 240 million people globally, including about 18% of women and 10% of men in the aged population (60 years old), and OA is expected to be the single greatest cause of disability in the common population by 2030 [3]. The imbalance between catabolic and anabolic factors in joints and inflammation causes pervasive cartilage damage, which is crucial to the progression of OA. Increasing evidence suggests that synovial inflammation is correlated with the pathogenesis and progression of OA, and local inflammatory responses plays a decisive role in the OA development [4]
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