Obtusifolin, an Anthraquinone Extracted from Senna obtusifolia (L.) H.S.Irwin & Barneby, Reduces Inflammation in a Mouse Osteoarthritis Model
| Autor: | Cheol-Ho Pan, Dong-Won Seol, Siyoung Yang, Jiho Nam, Choong-Gu Lee, Gabbine Wee |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
MMP3 obtusifolin Pharmaceutical Science lcsh:Medicine lcsh:RS1-441 Inflammation Osteoarthritis Pharmacology Matrix metalloproteinase Article NF-κB lcsh:Pharmacy and materia medica 03 medical and health sciences 0302 clinical medicine In vivo Drug Discovery medicine biology Chemistry Cartilage lcsh:R Interleukin medicine.disease osteoarthritis 030104 developmental biology medicine.anatomical_structure inflammation 030220 oncology & carcinogenesis biology.protein Molecular Medicine Cyclooxygenase medicine.symptom |
| Zdroj: | Pharmaceuticals, Vol 14, Iss 249, p 249 (2021) Pharmaceuticals |
| ISSN: | 1424-8247 |
| Popis: | Osteoarthritis (OA) is an age-related degenerative disease that causes cartilage dysfunction and inflammation. Obtusifolin, an anthraquinone extracted from Senna obtusifolia (L.) H.S.Irwin & Barneby seeds, has anti-inflammatory functions; it could be used as a drug component to relieve OA symptoms. In this study, we investigated the effects of obtusifolin on OA inflammation. In vitro, interleukin (IL)-1β (1 ng/mL)-treated mouse chondrocytes were co-treated with obtusifolin at different concentrations. The expression of matrix metalloproteinase (Mmp) 3, Mmp13, cyclooxygenase 2 (Cox2), and signaling proteins was measured by polymerase chain reaction and Western blotting; collagenase activity and the PGE2 level were also determined. In vivo, OA-induced C57BL/6 mice were administered obtusifolin, and their cartilage was stained with Safranin O to observe damage. Obtusifolin inhibited Mmp3, Mmp13, and Cox2 expression to levels similar to or more than those after treatment with celecoxib. Additionally, obtusifolin decreased collagenase activity and the PGE2 level. Furthermore, obtusifolin regulated OA via the NF-κB signaling pathway. In surgically induced OA mouse models, the cartilage destruction decreased when obtusifolin was administered orally. Taken together, our results show that obtusifolin effectively reduces cartilage damage via the regulation of MMPs and Cox2 expression. Hence, we suggest that obtusifolin could be a component of another OA symptom reliever. |
| Databáze: | OpenAIRE |
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