Department of Biochemistry and Molecular Biology, Institute of Basic Medicine, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, PR China.
Pharm Biol. 2011 Aug;49(8):815-20. doi: 10.3109/13880209.2010.550055. Epub 2011 Apr 18.
Inula britanica Linn. (Compositae) is a traditional Chinese medicinal herb that has been used to treat bronchitis and inflammation. The total flavonoid extracts (TFEs) isolated from its flowers can inhibit neointimal formation induced by balloon injury in vivo.
To investigate the mechanism by which TFE suppresses oxidative stress generation and the subsequent inflammation response in vitro.
The cultured vascular smooth muscle cells (VSMCs) form rats were exposed to oxidative stress following pretreatment with or without TFE at different concentration. Then, fluorescence staining was used to detect superoxide anion (O₂(˙-)) production, and the lever of maleic dialdehyde (MDA) and superoxide dismutase (SOD) was measured at the same time. Furthermore, tumor necrosis factor-α (TNF-α) was measured by enzyme linked immunosorbent assay (ELISA), reverse transcription-PCR and western blot were performed to detect the expression activity of p47(phox) gene, and immunoprecipitation was used to test the level of p47(phox) phosphorylation.
TFE inhibited the production of O₂(˙-) induced by H₂O₂ in VSMCs, with decrease in secretion of TNF-α; elevated the activity of SOD in the medium, similar to the effect of quercetin; reduced the level of MDA in culture medium of VSMCs. The pretreatment with TFE resulted in decrease the level of p47(phox) mRNA and protein, and even p47(phox) phosphorylation in VSMCs, compared with H₂O₂ control.
These findings demonstrate that TFE is capable of attenuating the oxidative stress generation and the subsequent inflammation response via preventing the overexpression and activation of p47(phox) and the increased TNF-α secretion in VSMCs in vitro.
旋覆花（菊科）是一种传统的中药，用于治疗支气管炎和炎症。从其花中分离得到的总黄酮提取物（TFE）可抑制体内球囊损伤诱导的新生内膜形成。
研究 TFE 抑制体外氧化应激产生及其随后炎症反应的机制。
用不同浓度的 TFE 预处理培养的大鼠血管平滑肌细胞（VSMCs），使其暴露于氧化应激下。然后，荧光染色检测超氧阴离子（O₂(˙-））的产生，同时测量丙二醛（MDA）和超氧化物歧化酶（SOD）的水平。此外，通过酶联免疫吸附试验（ELISA）检测肿瘤坏死因子-α（TNF-α），反转录-聚合酶链反应（RT-PCR）和蛋白质印迹法（Western blot）检测 p47(phox)基因的表达活性，免疫沉淀法检测 p47(phox)磷酸化水平。
TFE 抑制 H₂O₂诱导的 VSMCs 中 O₂(˙-)的产生，减少 TNF-α的分泌；提高培养基中 SOD 的活性，作用类似于槲皮素；降低 VSMCs 培养基中 MDA 的水平。与 H₂O₂对照相比，TFE 预处理可降低 VSMCs 中 p47(phox)mRNA 和蛋白水平，甚至 p47(phox)磷酸化水平。
这些发现表明，TFE 能够通过防止 p47(phox)的过度表达和激活以及减少 TNF-α的分泌，减轻 VSMCs 中的氧化应激产生及其随后的炎症反应。
