Ginsenoside Ro suppresses interleukin-1β-induced apoptosis and inflammation in rat chondrocytes by inhibiting NF-κB  

作　　者：ZHANG Xiao-Hong XU Xian-Xiang XU Tao 

机构地区：[1]School of Biomedical Science, Huaqiao University

出　　处：《Chinese Journal of Natural Medicines》2015年第4期283-289,共7页中国天然药物（英文版）

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);the Special Fund for Basic Scientific Research of Central Colleges,Huaqiao University(No.JB-SJ1012);the Science Foundation of Huaqiao University(No.10HZR28)

摘　　要：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.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.

关 键 词：Ginsenoside Ro Cbondrocytes Apoptosis INFLAMMATION NF-ΚB 

分 类 号：R965[医药卫生—药理学]