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 （...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-κ3 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-κ3 p65 phosphorylation induced by 1L-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-κ3 signal pathway. Therefore, we propose that Ro might be a potential novel drug for the treatment ofosteoarthritis.展开更多
基金supported by the Key Science and Technology Project of Fujian Province(No.2012Y0049)the Key Project of Quanzhou City Science and Technology Program(No.2011Z8)+1 种基金the Special Fund for Basic Scientific Research of Central Colleges,Huaqiao University(No.JB-SJ1012)the Science Foundation of Huaqiao University(No.10HZR28)
文摘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-κ3 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-κ3 p65 phosphorylation induced by 1L-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-κ3 signal pathway. Therefore, we propose that Ro might be a potential novel drug for the treatment ofosteoarthritis.
