1,25(OH)2D3 promotes chondrocyte apoptosis and restores physical function in rheumatoid arthritis through the NF-κB signal pathway

Publication date: October 2018Source: Biomedicine & Pharmacotherapy, Volume 106Author(s): Run Tian, Xiaofang Li, Yue Li, Kunzheng Wang, Chunsheng Wang, Pei YangAbstractWe explored the modulatory effect of 1,25(OH)2D3 on chondrocytes and physical function in rats with RA and its mechanism underlying the regulation of NF-κB signal pathway. RA patients and healthy volunteers were selected. Sprague-Dawley (SD) rats were used to establish RA models. The paw volume of rats was estimated. Chondrocytes were isolated from RA rats. The protein levels in both cartilage tissues and chondrocytes were determined using western blotting. Apoptosis was evaluated using TUNEL assay. Serum levels of IL-1β, IL-6, IL-10 and IL-17 were measured by enzyme-linked immunosorbent assay (ELISA). Serum levels of 1,25(OH)2D3 were lower in RA patients than in healthy volunteers. Rats in the RA + VD3 group were lighter than those in normal and PBS groups, with an increased paw volume, severer joint swelling, higher expression levels of p-IκBα, p-p65, IL-1β, IL-6, and IL-17, and lower expression level of IL-10, while those in RA and RA + VD3 + NF-κB group differed more significantly. In addition, by comparing RA rats and RA + NF-κB rats, we found that TNF-α stimulation exacerbated RA, increased expression levels of p-IκBα, p-p65, IL-1β, IL-6, and IL-17, and decreased the expression level of IL-10. Compared with RA chondrocytes, chondrocytes from RA + VD3 rats exhibited lower express...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research