Quyu Shengxin capsule (QSC) inhibits Ang-II-induced abnormal proliferation of VSMCs by down-regulating TGF-β, VEGF, mTOR and JAK-STAT pathways.

ETHNOPHARMACOLOGICAL RELEVANCE: 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.

AIM OF STUDY: 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.

MATERIALS AND METHODS: 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) (10-7 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.

RESULTS: 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.

CONCLUSION: 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.