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血管平滑肌细胞(VSMC)过度增殖是多种血管疾病发生的根本原因,黄芩苷作为一种传统植物天然药物,具有抗菌、消炎以及保护血管等多种功能。本研究采用细胞学及分子生物学手段,通过CCK-8法检测不同浓度的黄芩苷(0μmol/L,50μmol/L和100μmol/L)对VSMC增殖的作用,同时测定增殖细胞核抗原PCNA的转录水平,进一步对VSMC增殖进行基因水平上的验证。同时,对MAPK信号通路中的关键因子ERK的表达量进行定量检测,分析黄芩苷调控VSMC增殖的信号通路。结果显示黄芩苷对VSMC增殖具有抑制作用,且呈药物剂量依赖效应;此外,VSMC中ERK的表达水平也随黄芩苷使用浓度增大而降低,从而推测黄芩苷可能通过调控ERK介导的相关信号途径实现对VSMC增殖的阻抑,达到防止血管发生病变的目的。此研究对保护血管功能和开发治疗血管疾病新药物具有积极的意义,也为代谢工程在天然药物开发方面的应用提供理论依据和实践基础。
Hypervascular proliferation of vascular smooth muscle cells (VSMCs) is the root cause of many vascular diseases. As a traditional natural medicine, baicalin has many functions such as anti-bacterial, anti-inflammatory and blood vessel protection. In this study, the effects of different concentrations of baicalin (0μmol / L, 50μmol / L and 100μmol / L) on the proliferation of VSMC were determined by CCK-8 assay by cytology and molecular biology methods. The transcription level of proliferating cell nuclear antigen PCNA , Further VSMC proliferation gene level validation. At the same time, we quantitatively detected the expression of ERK, a key factor in MAPK signaling pathway, and analyzed the signal pathway that baicalin regulates VSMC proliferation. The results showed that baicalin inhibited the proliferation of VSMC in a dose-dependent manner. In addition, the expression of ERK in VSMC also decreased with the increase of baicalin concentration, suggesting that baicalin could regulate ERK-mediated signal transduction Way to achieve VSMC proliferation inhibition, to prevent the occurrence of angiogenic purposes. This study is of great significance to the protection of vascular function and the development of new drugs for the treatment of vascular diseases. It also provides a theoretical basis and a practical basis for the application of metabolic engineering in the development of natural medicines.