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ABSTRACT
The aim of this study was to investigate the effects and underlying mechanisms of calcitonin (CT) on interleukin 1 beta (IL-1β) stimulated human chondrocytes. IL-1β (5 ng/mL) was added into chondrocytes to establish osteoarthritis (OA) model in vitro. Different concentrations of CT (0.1, 0.5, 1, 5, 10 and 50 nM) were used for treating IL-1β stimulated chondrocytes. Cell viability of chondrocytes was measured by cell counting kit-8 (CCK8) method. Western blotting was performed to evaluate the expression of matrix metalloproteinases (MMP-13), tissue inhibitor of metalloproteinases 1 (TIMP-1), p50 and p38. CT inhibited MMP-13 expression and promoted TIMP-1 expression in the IL-1β stimulated human chondrocytes. The CT-mediated alteration of MMP-13/TIMP-1 ratio was partially attributed to the inactivation of the p50- nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by suppressing p50 in IL-1β stimulated chondrocytes. CT might play a protective role in IL-1β stimulated OA model via p50-NF-κB pathway.
Abbreviations: CT: calcitonin; IL-1β: interleukin-1β; MMP-13: matrix metalloproteinases-13; TIMP-1: tissue inhibitors of metalloproteinases-1.
Graphical Abstract
CT regulates expression of MMP 13/ TIMP-1 via p50-NF-κB pathway.
Authors’ Contribution
Xiaodong Bai was carried out the literature research, clinical studies, experimental studies, data acquisition, data analysis, statistical analysis, manuscript preparation and manuscript preparation; Ai Guo was dedicated to the the entire study and study design; Yadong Li was involved in the definition of intellectual content and manuscript review. All authors have read and approved this article.
Disclosure statement
No potential conflict of interest was reported by the authors.