Ginsenoside Ro suppresses interleukin-1β-induced apoptosis and inflammation in rat chondrocytes by inhibiting NF-κB.
10.1016/S1875-5364(15)30015-7
- Author:
Xiao-Hong ZHANG
1
;
Xian-Xiang XU
2
;
Tao XU
1
Author Information
1. School of Biomedical Science, Huaqiao University, Quanzhou 362021, China.
2. School of Biomedical Science, Huaqiao University, Quanzhou 362021, China. Electronic address: xuxianxiang@163.com.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Chondrocytes;
Ginsenoside Ro;
Inflammation;
NF-κB
- MeSH:
Animals;
Anti-Inflammatory Agents;
pharmacology;
Apoptosis;
drug effects;
Apoptosis Regulatory Proteins;
drug effects;
metabolism;
Caspase 3;
metabolism;
Cell Survival;
drug effects;
Chondrocytes;
cytology;
drug effects;
Cyclooxygenase 2;
drug effects;
metabolism;
Down-Regulation;
drug effects;
Drug Evaluation, Preclinical;
Ginsenosides;
pharmacology;
Inflammation;
chemically induced;
drug therapy;
Interleukin-1beta;
antagonists & inhibitors;
pharmacology;
Matrix Metalloproteinase 3;
drug effects;
metabolism;
Matrix Metalloproteinase 9;
drug effects;
NF-kappa B;
antagonists & inhibitors;
drug effects;
metabolism;
Phosphorylation;
drug effects;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
drug effects
- From:
Chinese Journal of Natural Medicines (English Ed.)
2015;13(4):283-289
- CountryChina
- Language:English
-
Abstract:
This study investigated effects of Ginsenoside Ro (Ro) on interleukin-1β (IL-1β)-induced apoptosis and inflammation in rat chondrocytes. The rat chondrocytes were co-treated with IL-1β (10 ng·kg(-1)) and Ro (50, 100 and 200 μmol·L(-1)) for 48 h. Chondrocytes viability was detected by the MTT assay and Annexin V-FITC/PI dual staining assay. Caspase 3 activity was measured by using caspase 3 colorimetric assay kit. Apoptosis related proteins Bax, Bad, Bcl-xL, PCNA, p53 and phospho-p53, along with inflammation related protein MMP 3, MMP 9 and COX-2, and the expression of phospho-NF-κB p65 were assayed by western blotting analyses. Ro could improve IL-1β-induced chondrocytes viability. Ro could suppress IL-1β-induced apoptosis by inhibiting levels of Bax and Bad, decreasing p53 phosphorylation and promoting the expression of Bcl-xL and PCNA. Ro inhibited caspase 3 activity. IL-1β-induced inflammation and matrix degration were also alleviated by Ro with down-regulating the expression of MMP 3, MMP 9 and COX-2. Moreover, Ro inhibited NF-κB p65 phosphorylation induced by IL-1β. In conclusion, these results suggested Ro exerted anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway. Therefore, we propose that Ro might be a potential novel drug for the treatment of osteoarthritis.
