کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5832426 | 1122597 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Celastrol attenuates bone erosion in collagen-Induced arthritis mice and inhibits osteoclast differentiation and function in RANKL-induced RAW264.7
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کلمات کلیدی
MMP-9M-CSFCTSKTRAPCTRALTRANKLPBSMAPK - MAPKcollagen-induced arthritis - آرتروز ناشی از کلاژنRheumatoid arthritis - آرتریتروماتوئیدaminotransferase - آمینوترانسفرازOsteoclast - استخوانکاه، استئوکلاستtartrate-resistant acid phosphatase - اسید فسفاتاز مقاوم در برابر تارتاتIntraperitoneally - داخل صفاقیCelastrol - سلسترولCIA - سیاPhosphate buffered saline - فسفات بافر شورmatrix metallopeptidase 9 - ماتریکس متالوپپتیداز 9macrophage colony-stimulating factor - ماکروفاژ عامل کلونی تحریک کنندهculture medium - محیط کشتCathepsin K - کتهفسین کmitogen-activated protein kinases - کیناز پروتئین فعال Mitogencalcitonin receptor - گیرنده کلسی تونین
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Recently, the traditional Chinese medicine Tripterygium wilfordii Hook f (TwHF) of the Celastraceae family has attracted increasing attention for its potential therapeutic application in patients with rheumatoid arthritis (RA). It is well accepted that TwHF exerts the antirheumatic activity and mainly depends on its potent anti-inflammatory property. To further explore the therapeutic potential of the well-defined TwHF-derived single compound - celastrol in RA, we study the therapeutic efficacy of celastrol on bone erosion in collagen-induced arthritis (CIA) mice and delineate its effects on osteoclast differentiation and functions in RANKL-induced osteoclast precursors RAW264.7 cell line. In CIA mice, daily injection of celastrol (beginning on day 28 after arthritis induction) markedly suppressed arthritis, and reduced bone damage in the joints as demonstrated by histology and bone micro-computed tomography (CT). The effects were accompanied by reductions of osteoclast cells in joints, serum tartrate-resistant acid phosphatase (TRAP) 5b, and expression of osteoclastic genes (Trap, Ctsk, Ctr, Mmp-9) and transcriptional factors (c-Fos, c-Jun and NFATc1). When RAW264.7 cells were treated with RANKL, celastrol inhibited the formation of TRAPÂ + multinucleated cells and the bone-resorbing activity in dose-dependent manners. Furthermore, celastrol reduced the RANKL-induced expression of osteoclastic genes and transcriptional factors, as well as phosphorylation of NF-kB and mitogen-activated protein kinases (MAPK). These findings show that celastrol could directly inhibit osteoclast formation and function, suggesting a novel therapeutic strategy of celastrol for managing RA, especially in preventing bone destruction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 24, Issue 2, February 2015, Pages 239-246
Journal: International Immunopharmacology - Volume 24, Issue 2, February 2015, Pages 239-246
نویسندگان
Ke Gan, Lingxiao Xu, Xiaoke Feng, Qiande Zhang, Fang Wang, Miaojia Zhang, Wenfeng Tan,