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APS relieves LPS-induced injury in ATDC5 cells;
APS down-regulates miR-92a expression;
KLF4 is a target gene of miR-92a;
Protective effects of APS are attenuated by KLF4 siRNA.
Astragalus polysaccharide (APS) is a traditional Chinese herbal medicine with anti-inflammatory and anti-aging activities.
This study aimed to explore the effect and associated mechanisms of APS on LPS-induced injury in ATDC5 cells, to evaluate the potential of APS for use as an adjuvant therapy for osteoarthritis (OA).
Materials and Methods
ATDC5 cells were pre-treated with APS and stimulated with lipopolysaccharide (LPS). Cell viability, ROS generation as well as the expression of IL-6, TNF-α, iNOS and Cox-2 were evaluated by performing CCK8 assay, ROS detection, ELISA, western blot and qRT-PCR. The expression of NF-κB and p38MAPK signal pathways related proteins and KLF4 was measured through western blot.
LPS increased the expression of IL-6 and TNF-α, elevated the expression of Cox-2, iNOS and increased ROS generation. APS treatment significantly alleviated LPS-induced damage in ATDC5 cells. Besides, miR-92a was down-regulated while KLF4 was up-regulated by APS. At the same time, the targeting relationship between miR-92a and KLF4 was demonstrated. The inhibitory effects of APS on LPS-induced injury in ATDC5 cells were attenuated by the combination of KLF4 siRNA. In addition, LPS induced NF-κB and p38MAPK signal pathways were decreased by APS treatment. Also, the inhibitory effect of APS on NF-κB and p38MAPK signal pathways was reversed by KLF4 siRNA.
The present study reveals that APS protects ATDC5 cells against LPS induced-injury by regulation of miR-92a/KLF4 axis and suppressing NF-κB and p38MAPK signal pathways.Le texte complet de cet article est disponible en PDF.
Keywords : Astragalus polysaccharide, Osteoarthritis, MiR-92a, KLF4
Vol 118Article 109180- octobre 2019 Retour au numéro
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