Inhibitory effect of oleanolic acid on inflammatory response in IL-1β-stimulated human synovial sarcoma SW982 cells
10.16438/j.0513-4870.2016-0610
- VernacularTitle:齐墩果酸对IL-1β诱导的SW982细胞炎症反应的抑制作用
- Author:
Jun-jiang LIAN
1
;
Bin-feng CHENG
1
;
Yao-xin GAO
1
;
Ya-ping ZHANG
1
;
Shuang-ping MA
1
;
Bin-bin ZHANG
1
;
Dan-dan GUO
1
;
Han XUE
1
;
Zhi-wei FENG
1
Author Information
1. College of Life Science and Technology, Xinxiang Medical University, Xinxiang 453003, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
oleanolic acid;
SW982 cell;
anti-inflammatory effect;
signal pathway;
inflammatory cytokine
- From:
Acta Pharmaceutica Sinica
2016;51(11):1711-
- CountryChina
- Language:Chinese
-
Abstract:
To study the role of oleanolic acid on interleukin (IL)-1β-stimulated expression of inflammatory cytokines, and to explore its anti-inflammatory mechanism in SW982 cells, the toxicity of oleanolic acid on SW982 cells was detected by MTT; effects of different concentrations of oleanolic acid (5, 10, 20 μmol·L-1) on the expression of inflammatory factors IL-6, IL-8 and matrix metalloproteinase-1 (MMP-1) was tested at protein and mRNA levels. The study was performed in IL-1β-stimulated SW982 cells together with enzyme-linked immunosorbent assay (ELISA) and real-time fluorescence quantitative PCR (real-time PCR) methods; the influence of oleanolic acid on the phosphorylation of mitogen-activated protein kinase (MAPK), phosphatidyl inositol-3-kinase/Akt (PI3K/Akt) and nuclear transcription factor-κB (NF-κB) signaling pathways related protein was analyzed by Western blot. Results showed that different concentrations of oleanolic acid (≤ 40 μmol·L-1) were almost non-toxicity to SW982 cells; oleanolic acid significantly inhibited the expression of inflammatory factors in a dose-dependent manner; oleanolic acid restrained extracellular signal-related kinase (ERK), p38, c-jun N-terminal kinase (JNK) and Akt protein phosphorylation and IκB-α protein degradation obviously. The inhibition effect of oleanolic acid on inflammatory factors stimulated by IL-1β may be worked through MAPK, PI3K/Akt and NF-κB signaling pathways.
