Lian Jun-jiang, Cheng Bin-feng, Gao Yao-xin, Zhang Ya-ping, Ma Shuang-ping, Zhang Bin-bin, Guo Dan-dan, Xue Han, Feng Zhi-wei
Yao Xue Xue Bao. 2016 Nov;51(11):1711-6.
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 m RNA 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.
为研究齐墩果酸对白细胞介素（IL）-1β刺激的炎性细胞因子表达的作用，并探讨其在SW982细胞中的抗炎机制，采用MTT法检测齐墩果酸对SW982细胞的毒性；采用酶联免疫吸附测定（ELISA）和实时荧光定量PCR（实时PCR）方法，检测不同浓度（5、10、20 μmol·L⁻¹）齐墩果酸对炎性因子IL-6、IL-8和基质金属蛋白酶-1（MMP-1）在蛋白和mRNA水平表达的影响。本研究在IL-1β刺激的SW982细胞中进行；采用蛋白质印迹法分析齐墩果酸对丝裂原活化蛋白激酶（MAPK）、磷脂酰肌醇-3激酶/Akt（PI3K/Akt）和核转录因子-κB（NF-κB）信号通路相关蛋白磷酸化的影响。结果显示，不同浓度（≤40 μmol·L⁻¹）的齐墩果酸对SW982细胞几乎无毒性；齐墩果酸能显著抑制炎性因子的表达，且呈剂量依赖性；齐墩果酸明显抑制细胞外信号调节激酶（ERK）、p38、c-Jun氨基末端激酶（JNK）和Akt蛋白的磷酸化以及IκB-α蛋白的降解。齐墩果酸对IL-1β刺激的炎性因子的抑制作用可能是通过MAPK、PI3K/Akt和NF-κB信号通路实现的。
