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Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Stress+Chaperones 2017 ; 22 (6): 767-74 Nephropedia Template TP
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Protective effects of Nebivolol against interleukin-1? (IL-1?)-induced type II collagen destruction mediated by matrix metalloproteinase-13 (MMP-13) #MMPMID28512729
Li Z; Liu B; Zhao D; Wang B; Liu Y; Zhang Y; Tian F; Li B
Cell Stress Chaperones 2017[Nov]; 22 (6): 767-74 PMID28512729show ga
The pathological progression of osteoarthritis (OA) involves degradation of articular cartilage matrix. Type II collagen is the main component of cartilage matrix, which is degraded by pro-inflammatory cytokines such as IL-1? mediated by MMP-13. Nebivolol, a licensed drug used for the treatment of hypertension in clinics, displays its anti-inflammatory capacity in various conditions. However, whether Nebivolol has a protective effect on cartilage matrix degradation has not been reported before. In this study, we investigated the effects of Nebivolol on regulating the expression of MMP-13 and degradation of type II collagen. Our results indicate that Nebivolol alleviated the increase in gene expression, protein expression, and activity of MMP-13 induced by IL-1?. Importantly, IL-1? strikingly reduced the levels of type II collagen in cell culture supernatants, which was reversed by treatment with Nebivolol in a dose-dependent manner. Mechanistically, Nebivolol was found to alleviate the increased levels of phosphorylated I?B? and reduced levels of total I?B? induced by IL-1?, which subsequently mitigated p65 nuclear translocation and the transcriptional activity of NF-?B. Furthermore, our results indicated that IL-1? treatment resulted in a significant increase in expression of the transcriptional factor interferon regulatory factor-1 (IRF-1) at both the mRNA and protein levels, which was significantly ameliorated by treatment with Nebivolol. The combination of these findings suggests that Nebivolol can potentially be applied in human OA treatment.