摘要
Objective： To investigate effects of Dahuang Zhechong Pill （大黄庶虫丸, DHZCP） on the cell cycle and the related signal pathways in vascular smooth muscle cells （VSMCs） stimulated by platelet-derived growth factor （PDGF） with the method of serum pharmacology. Methods： DNA synthesis in VSMCs was examined by detecting 5＇-bromo-2＇-deoxyuridine incorporation with the immunocytochemical method. The cycle of VSMCs was evaluated with flow cytometry. Expressions of cyclin D1, p27, protein kinase C α （PKC α）, and phosphorylated extracellular signal regulated kinase 1/2 （ERK1/2） were quantified by Western blot method. Results： DHZCP containing serum significantly inhibited DNA synthesis of PDGF-stimulated VSMCs, arrested the cells in G1 phase, modulated the protein expressions of cyclin D1 and p27, and suppressed the activation of PKC α and ERK1/2. Conclusion： DHZCP containing serum inhibits VSMCs proliferation via modulating the expressions of cell cycle proteins to arrest the cell in G1 phase, which is attributed to, at least in part, suppressing PKC α -ERK1/2 signaling in VSMCs.
Objective： To investigate effects of Dahuang Zhechong Pill （大黄庶虫丸, DHZCP） on the cell cycle and the related signal pathways in vascular smooth muscle cells （VSMCs） stimulated by platelet-derived growth factor （PDGF） with the method of serum pharmacology. Methods： DNA synthesis in VSMCs was examined by detecting 5＇-bromo-2＇-deoxyuridine incorporation with the immunocytochemical method. The cycle of VSMCs was evaluated with flow cytometry. Expressions of cyclin D1, p27, protein kinase C α （PKC α）, and phosphorylated extracellular signal regulated kinase 1/2 （ERK1/2） were quantified by Western blot method. Results： DHZCP containing serum significantly inhibited DNA synthesis of PDGF-stimulated VSMCs, arrested the cells in G1 phase, modulated the protein expressions of cyclin D1 and p27, and suppressed the activation of PKC α and ERK1/2. Conclusion： DHZCP containing serum inhibits VSMCs proliferation via modulating the expressions of cell cycle proteins to arrest the cell in G1 phase, which is attributed to, at least in part, suppressing PKC α -ERK1/2 signaling in VSMCs.
基金
Supported by the National Natural Science Foundation of China (No.30572347)
