Antiarthritic Effects of Sorafenib in Rats with Adjuvant-Induced Arthritis
Autor: | Zhen-Zhen Wang, Xue-Ying Huang, Xiao-Ming Zhang, Tian-Yu Huang, Yong-Fang Gong, Fei Liu |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Sorafenib Histology business.industry Fibroblast growth factor receptor 1 Inflammation Pharmacology medicine.disease 03 medical and health sciences 030104 developmental biology medicine.anatomical_structure In vivo Rheumatoid arthritis medicine Tumor necrosis factor alpha Intradermal injection Anatomy medicine.symptom Synovial membrane business Ecology Evolution Behavior and Systematics Biotechnology medicine.drug |
Zdroj: | The Anatomical Record. 301:1519-1526 |
ISSN: | 1932-8486 |
Popis: | Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting the synovial membrane of joints. In this study, we aimed to investigate whether sorafenib exerts antiarthritic effects on RA in vivo. Adjuvant arthritis (AA) was induced (day 0) in male Sprague-Dawley rats by intradermal injection of 0.1 mL of complete Freund's complete adjuvant into the left hind paw. Sorafenib (10, 20, or 40 mg/kg/day) was administered intragastrically from day 10 to 24. Body weight, paw volume, synovial inflammation, and tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-10, and IL-17 serum levels were detected. In addition, microvascular density (MVD) and the expression of vascular endothelial growth factor receptor 2 (VEGFR-2) and fibroblast growth factor receptor 1 (FGFR-1) in synovial tissues were analyzed. Our data revealed that sorafenib administration led to significant body weight gain in AA rats but suppressed paw swelling, synovial hyperplasia, and inflammatory infiltration. Furthermore, it decreased TNF-α, IL-1β, and IL-17 serum levels and upregulated IL-10. MVD and VEGFR-2 and FGFR-1 expression in synovial tissues were significantly reduced. Thus, this study shows that sorafenib exerts anti-arthritic effects in AA rats and therefore has potential in RA treatment. Anat Rec, 301:1519-1526, 2018. © 2018 Wiley Periodicals, Inc. |
Databáze: | OpenAIRE |
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