Curcumin inhibits LPS-induced inflammation in VSMCs via Toll-like receptor 4/NADPH oxidase/reactive oxygen species signaling pathway
10.7652/jdyxb201504024
- VernacularTitle:姜黄素对内毒素诱导的血管平滑肌细胞Toll 样受体4/NADPH 氧化酶/活性氧信号通路及炎症因子释放的影响
- Author:
Haijie ZHAI
;
Zhe MENG
;
Hailong TAO
;
Zhongle BAI
;
Chao YAN
;
Ling LI
- Publication Type:Journal Article
- Keywords:
curcumin;
Toll-like receptor 4 (TLR4);
reactive oxygen species (ROS);
tumor necrosis factor-α(TNF-α);
interleukin-1 (IL-1);
inflammation;
TLR4/NADPH oxidase/ROS signaling pathways
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
2015;(4):543-548
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the inhibitory effect of curcumin on LPS-induced inflammation and the activation of Toll-like receptor 4 (TLR4 )/NADPH oxidase/reactive oxygen species (ROS)signaling pathway in vascular smooth muscle cells (VSMCs).Methods Primary VSMCs were cultured and divided into control group, LPS group,LPS + curcumin 5 μmol/L group,LPS + curcumin 10 μmol/L group and LPS + curcumin 30 μmol/L group.Cell activity was observed by MTT assay.The secretion of tumor necrosis factor-α(TNF-α)and interleukin-1 (IL-1)was measured by enzyme linked immunosorbent assay (ELISA)kits.The mRNA expressions of TLR4 and p22phox were detected by real-time PCR.Expression of intracellular ROS was measured by flow cytometry. Results The activities of VSMCs were not significantly affected by curcumin at the concentration between 0 and 80 μmol/L.Curcumin (5,10 and 30 μmol/L)significantly inhibited LPS-induced oversecretion of TNF-αand IL-1, as well as overexpression of TLR4 and p22phox at the mRNA and protein levels,and ROS production in VSMCs in a concentration-dependent manner.Conclusion Curcumin has a concentration-dependent inhibitory effect on the secretion of inflammatory cytokine,overexpressions of TLR4 and p22phox,and production of ROS in VSMCs stimulated by LPS.Furthermore,curcumin may partly depend on TLR4/NADPH oxidase/ROS signaling pathways to inhibit inflammation in LPS-induced VSMCs.