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1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway

Sun, Hua-Qiang ; Yan, Dong ; Wang, Qin-Nan ; Meng, Hong-Zheng ; Zhang, Ye-Yong ; Yin, Lu-Xu ; Yan, Xin-Feng ; Li, Shu-Feng

Journal of bone and mineral metabolism, 2019-05, Vol.37 (3), p.430-440 [Periódico revisado por pares]

Tokyo: Springer Japan

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Título:
1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway
Autor: Sun, Hua-Qiang ; Yan, Dong ; Wang, Qin-Nan ; Meng, Hong-Zheng ; Zhang, Ye-Yong ; Yin, Lu-Xu ; Yan, Xin-Feng ; Li, Shu-Feng
Assuntos: Animals ; Apoptosis ; Apoptosis - drug effects ; Arthritis ; Arthritis, Experimental - diagnostic imaging ; Arthritis, Experimental - drug therapy ; Arthritis, Experimental - metabolism ; Arthritis, Experimental - pathology ; Arthritis, Rheumatoid - drug therapy ; Calcitriol ; Cell proliferation ; Cell Proliferation - drug effects ; Cells, Cultured ; Down-Regulation - drug effects ; Hyperplasia ; Inflammation - pathology ; Inflammation Mediators - metabolism ; Inflammatory diseases ; Injection ; Joint diseases ; Latency ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; NF-kappa B - metabolism ; NF-κB protein ; Original Article ; Orthopedics ; Rats, Sprague-Dawley ; Rheumatoid arthritis ; Rodents ; Severity of Illness Index ; Signal transduction ; Signal Transduction - drug effects ; Synovial Membrane - drug effects ; Synovial Membrane - pathology ; Synoviocytes ; Synoviocytes - drug effects ; Synoviocytes - metabolism ; Synoviocytes - pathology ; Vitamin D - analogs & derivatives ; Vitamin D - pharmacology ; Vitamin D - therapeutic use ; Vitamin D3
É parte de: Journal of bone and mineral metabolism, 2019-05, Vol.37 (3), p.430-440
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SourceType-Scholarly Journals-1
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Descrição: An aggressive proliferation of synoviocytes is the hallmark of rheumatoid arthritis (RA). Emerging evidence shows that inhibiting the NF-κB signaling pathway with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] may be a therapeutic approach for controlling inflammatory diseases. In this study, we demonstrated the protective effects of three different 1,25(OH)2D3 concentration on adjuvant-induced arthritis (AA) rats through the NF-κB signaling pathway and their pro-apoptotic roles in cultured adjuvant-induced arthritis synoviocytes (AIASs). AA rats were prepared by injecting complete Freund’s adjuvant and independently given daily intraperitoneal injection of 1,25(OH)2D3 at concentrations of 50, 100, and 300 ng/day/kg. Subsequently, AIASs were isolated from the inflamed joints of AA rats to test the effects of 1,25(OH)2D3 on AIASs in vitro. Intraperitoneal injection of 1,25-(OH)2D3 was found to induce a concentration- and time-dependent improvement in relieving the symptoms of AA. We found an increased paw withdrawal thermal latency (PWTL) in the affected paw of AA rats as the concentration of 1,25-(OH)2D3 increased. 1,25-(OH)2D3 treatment reduced levels of inflammatory factors in synovial tissues of AA rats. In the case of cultured AIASs, 1,25-(OH)2D3 was shown to inhibit cell proliferation and induce cell apoptosis in a concentration-dependent manner. Additionally, 1,25-(OH)2D3 inhibited the activation of the NF-κB signaling pathway. In conclusion, our study provides evidence emphasizing that 1,25(OH)2D3 has the potential to attenuate disease severity in RA potentially due to its contributory role in synoviocyte proliferation and apoptosis. The protective role of 1,25(OH)2D3 against RA depends on the NF-κB signaling pathway.
Editor: Tokyo: Springer Japan
Idioma: Inglês

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1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway

Sun, Hua-Qiang ; Yan, Dong ; Wang, Qin-Nan ; Meng, Hong-Zheng ; Zhang, Ye-Yong ; Yin, Lu-Xu ; Yan, Xin-Feng ; Li, Shu-Feng

Tokyo: Springer Japan

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