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Polydatin Alleviates Lipopolysaccharide-Triggered Inflammatory Injury Through Up-Regulating miR-125b in Chondrogenic ATDC5 Cells

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Osteoarthritis is a bone-joint disease prevalent in older people characterized by joint inflammation. In traditional Chinese medicine, polydatin plays an important anti-inflammatory role. This study analyzed the potential effects and possible internal mechanisms of polydatin on osteoarthritis. First, lipopolysaccharide-induced osteoarthritis injury was established in chondrogenic ATDC5 cells. Lipopolysaccharides significantly stimulated inflammatory injuries in ATDC5 cells as exemplified by a decrease in cell viability and an increase in inflammatory cytokine secretions including interleukin-6, tumor necrosis factor-a, and interleukin-1. Moreover, lipopolysacchrides also increased Cleaved caspase-3 and Cleaved Poly (ADP-ribose) polymerase to promote cell apoptosis. Second, polydatin showed significant protective effects against lipopolysaccharide-induced inflammatory injury, again exemplified by increased cell viability, decreased inflammatory cytokines, Cleaved caspase-3, and Cleaved poly (ADP-ribose) polymerase. Lastly, miR-125b and its binding target Rho-Associated Coiled-Coil Containing Protein Kinase 1 were closely associated with regulatory effects of polydatin against lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries. Polydatin alleviated lipopolysaccharide-stimulated inflammatory injuries via the down-regulation of miR-125b. The present study concludes that polydatin plays an anti-inflammatory role in lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries via the down-regulation of miR-125b.
Title: Polydatin Alleviates Lipopolysaccharide-Triggered Inflammatory Injury Through Up-Regulating miR-125b in Chondrogenic ATDC5 Cells
Description:
Osteoarthritis is a bone-joint disease prevalent in older people characterized by joint inflammation.
In traditional Chinese medicine, polydatin plays an important anti-inflammatory role.
This study analyzed the potential effects and possible internal mechanisms of polydatin on osteoarthritis.
First, lipopolysaccharide-induced osteoarthritis injury was established in chondrogenic ATDC5 cells.
Lipopolysaccharides significantly stimulated inflammatory injuries in ATDC5 cells as exemplified by a decrease in cell viability and an increase in inflammatory cytokine secretions including interleukin-6, tumor necrosis factor-a, and interleukin-1.
Moreover, lipopolysacchrides also increased Cleaved caspase-3 and Cleaved Poly (ADP-ribose) polymerase to promote cell apoptosis.
Second, polydatin showed significant protective effects against lipopolysaccharide-induced inflammatory injury, again exemplified by increased cell viability, decreased inflammatory cytokines, Cleaved caspase-3, and Cleaved poly (ADP-ribose) polymerase.
Lastly, miR-125b and its binding target Rho-Associated Coiled-Coil Containing Protein Kinase 1 were closely associated with regulatory effects of polydatin against lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries.
Polydatin alleviated lipopolysaccharide-stimulated inflammatory injuries via the down-regulation of miR-125b.
The present study concludes that polydatin plays an anti-inflammatory role in lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries via the down-regulation of miR-125b.

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