Shibo Zou1, Changyin Wang1, Zhengjun Cui2, Pengfei Guo1, Qingnan Meng1, Xun Shi1, Ya Gao1, Gaoyuan Yang1, Zhaofeng Han1. 1. Department of Burn and Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. 2. Department of Burn and Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: zhengjuncui2006@163.com.
Abstract
BACKGROUND: β-Elemene is a natural anticancer compound extracted from the Chinese medicinal herb Curcuma Wenyujin. This study was done to determine the effect of β-elemene on the apoptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) and associated molecular mechanisms. METHODS: RA-FLS were treated for 72h with β-elemene at 10-200μg/ml and cell viability and apoptotic changes were examined. The involvement of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) was checked. RESULTS: We found that β-elemene significantly inhibited the viability and promoted apoptosis of RA-FLS in a concentration-dependent fashion. β-Elemene-treated FLS showed a significant decline in mitochondrial membrane potential, an accumulation of cytochrome c in the cytosol, and increased activities of caspase-9 and caspase-3. β-Elemene treatment caused an enhancement of p38 MAPK phosphorylation and ROS production. The pro-apoptotic activity of β-elemene was significantly reversed by pretreatment with the p38 inhibitor SB203580 or ROS inhibitor N-acetyl-l-cysteine. CONCLUSIONS: Taken together, β-elemene is effective in inducing mitochondrial apoptosis of RA-FLS, which is mediated through induction of ROS formation and p38 MAPK activation. β-Elemene may thus have therapeutic benefits for RA.
BACKGROUND: β-Elemene is a natural anticancer compound extracted from the Chinese medicinal herb Curcuma Wenyujin. This study was done to determine the effect of β-elemene on the apoptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) and associated molecular mechanisms. METHODS:RA-FLS were treated for 72h with β-elemene at 10-200μg/ml and cell viability and apoptotic changes were examined. The involvement of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) was checked. RESULTS: We found that β-elemene significantly inhibited the viability and promoted apoptosis of RA-FLS in a concentration-dependent fashion. β-Elemene-treated FLS showed a significant decline in mitochondrial membrane potential, an accumulation of cytochrome c in the cytosol, and increased activities of caspase-9 and caspase-3. β-Elemene treatment caused an enhancement of p38 MAPK phosphorylation and ROS production. The pro-apoptotic activity of β-elemene was significantly reversed by pretreatment with the p38 inhibitor SB203580 or ROS inhibitor N-acetyl-l-cysteine. CONCLUSIONS: Taken together, β-elemene is effective in inducing mitochondrial apoptosis of RA-FLS, which is mediated through induction of ROS formation and p38 MAPK activation. β-Elemene may thus have therapeutic benefits for RA.