Casticin inhibits PDGF-induced proliferation and migration of airway smooth muscle cells
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Updated: Feb 11, 2026

Measuring Proliferation of Vascular Smooth Muscle Cells Using Click Chemistry
Published on: October 30, 2019
Ying Dai1, Ruiduo Cheng1, Jie Gao1
1Department of Pediatrics, Henan University Huaihe Hospital, Kaifeng 475000, Henan Province, PR China.
Abstract:
Casticin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone), one of the main components from Vitex rotundifolia L., was reported to possess several pharmacological properties, including anti-inflammatory, hepatoprotective, anticancer, anti-asthma activities. However, the effects of casticin on airway smooth muscle cells (ASMCs) proliferation and migration have not been explored. This study aimed to evaluate the effects of casticin on the proliferation and migration of ASMCs, and study the possible molecular mechanism. Our results demonstrated that casticin significantly suppressed the proliferation and migration of ASMCs exposed to platelet-derived growth factor (PDGF), as well as reversed the PDGF-induced inhibition of the expression of contractile phenotype markers in ASMCs. In addition, casticin also inhibited PDGF-induced the expression of type I collagen and fibronectin in ASMCs induced by PDGF. Furthermore, casticin significantly prevented the activation of ERK1/2 and NF-κB pathways in PDGF-stimulated ASMCs. Taken together, these data demonstrated that casticin inhibits PDGF-induced human ASMC proliferation and migration through suppressing the activation of ERK1/2 and NF-κB signaling pathways.
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