Yu Jinjin, Li Weifeng, Zhao Lintao, Qiao Yuan, Yu Jiabao, Huang Qiuxia, Yang Yajie, Xiao Xin, Guo Dong
School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
J Ethnopharmacol. 2021 Jul 15;275:114112. doi: 10.1016/j.jep.2021.114112. Epub 2021 Apr 24.
Quyu Shengxin capsule (QSC) is an herbal compound commonly used to treat blood stasis syndrome in China, and blood stasis syndrome is considered to be the root of cardiovascular diseases (CVD) in traditional Chinese medicine. However, the potential molecular mechanism of QSC is still unknown.
To study the therapeutic effect of QSC on the abnormal proliferation of VSMCs induced by Ang-II, and to explore its possible mechanism of action.
Qualitative analysis and quality control of QSC through UPLC-MS/MS and UPLC. The rat thoracic aorta vascular smooth muscle cells (VSMCs) were cultured in vitro, and then stimulated with Angiotensin Ⅱ (Ang-II) (10 mol/L) for 24 h to establish a cardiovascular cell model. The cells were then treated with different concentrations of QSC drug-containing serum or normal goat serum. MTT assay was used to detect the viability of VSMCs and abnormal cell proliferation. In order to analyze the possible signal transduction pathways, the content of various factors in the supernatant of VSMCs was screened and determined by means of the Luminex liquid suspension chip detection platform, and the phosphoprotein profile in VSMCs was screened by Phospho Explorer antibody array.
Compared with the model group, serum cell viability and inflammatory factor levels with QSC were significantly decreased (P < 0.001). In addition, the expression levels of TGF-β, VEGF, mTOR and JAK-STAT in the QSC-containing serum treatment group were significantly lower than those in the model group. QSC may regulate the pathological process of CVD by reducing the levels of inflammatory mediators and cytokines, and protecting VSMCs from the abnormal proliferation induced by Ang-II.
QSC inhibits Ang-II-induced abnormal proliferation of VSMCs, which is related to the down-regulation of TGF-β, VEGF, mTOR and JAK-STAT pathways.
祛瘀生新胶囊（QSC）是中国常用于治疗血瘀证的一种草药复方，而血瘀证在传统中医中被认为是心血管疾病（CVD）的根源。然而，QSC的潜在分子机制仍不清楚。
研究QSC对血管紧张素II（Ang-II）诱导的血管平滑肌细胞（VSMC）异常增殖的治疗作用，并探讨其可能的作用机制。
通过超高效液相色谱-串联质谱法（UPLC-MS/MS）和超高效液相色谱法（UPLC）对QSC进行定性分析和质量控制。体外培养大鼠胸主动脉血管平滑肌细胞（VSMC），然后用血管紧张素II（Ang-II）（10 μmol/L）刺激24小时以建立心血管细胞模型。然后用不同浓度的含QSC药物血清或正常山羊血清处理细胞。采用MTT法检测VSMC的活力和异常细胞增殖。为了分析可能的信号转导途径，通过Luminex液体悬浮芯片检测平台筛选并测定VSMC上清液中各种因子的含量，并通过磷酸化蛋白探索者抗体芯片筛选VSMC中的磷酸化蛋白谱。
与模型组相比，QSC处理组的血清细胞活力和炎症因子水平显著降低（P < 0.001）。此外，含QSC血清处理组中转化生长因子-β（TGF-β）、血管内皮生长因子（VEGF）、哺乳动物雷帕霉素靶蛋白（mTOR）和Janus激酶-信号转导及转录激活因子（JAK-STAT）的表达水平明显低于模型组。QSC可能通过降低炎症介质和细胞因子水平，并保护VSMC免受Ang-II诱导的异常增殖，从而调节CVD的病理过程。
QSC抑制Ang-II诱导的VSMC异常增殖，这与TGF-β、VEGF、mTOR和JAK-STAT信号通路的下调有关。
