Shikimic acid prevents cartilage matrix destruction in human chondrocytes
| Autor: | Jining Shen, Xiaobin Guo, Yu Liu, Menglei Xu, Jiaxiang Bai, Houyi Sun, Binqing Yu, Liangliang Wang, Yuefeng Hao, Dechun Geng |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Immunology Type II collagen Shikimic Acid Osteoarthritis Matrix (biology) Extracellular matrix 03 medical and health sciences Chondrocytes 0302 clinical medicine Matrix Metalloproteinase 13 Disintegrin medicine Humans Immunology and Allergy Collagen Type II Cells Cultured Aggrecan 030203 arthritis & rheumatology Pharmacology Tissue Inhibitor of Metalloproteinase-2 Tissue Inhibitor of Metalloproteinase-1 biology Tumor Necrosis Factor-alpha Chemistry NF-kappa B medicine.disease In vitro Extracellular Matrix 030104 developmental biology ADAMTS4 Protein Cancer research biology.protein Matrix Metalloproteinase 3 Tumor necrosis factor alpha ADAMTS5 Protein Matrix Metalloproteinase 1 |
| Zdroj: | International Immunopharmacology. 63:155-160 |
| ISSN: | 1567-5769 |
| Popis: | Abnormal reduction of extracellular matrix (ECM), including type II collagen and aggrecan, caused by tumor necrosis factor-α (TNF-α) is an important pathological feature of osteoarthritis (OA). Shikimic acid (SA), derived from natural plants, has displayed effective pharmacological properties in diverse diseases. The biological roles of SA in OA have not been reported before. Here, we found that treatment with SA (1 mM, 10 mM) prevented TNF-α-induced degradation of type II collagen and aggrecan ECM in human primary chondrocytes culture in vitro. Importantly, we also reported that SA treatment reduced TNF-α-induced expression of matrix metalloproteinase‑1, ‑3, and ‑13 (MMP‑1, ‑3, and ‑13) and increased expression of tissue inhibitor of metalloproteinase‑1 and ‑2 (TIMP‑1, ‑2). Additionally, SA treatment attenuated TNF-α-induced expression of a disintegrin and metalloprotease‑4 and ‑5 (ADAMTS‑4, ‑5). Mechanistically, we found that SA prevented activation of the nuclear factor-κB (NF‑κB) pathway. Our findings suggest that SA might act as an important therapeutic agent in the treatment of OA. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect