Abelmoschus manihot Flower Extract Retards Platelet-Derived Growth Factor-BB-Stimulated Proliferation and Migration in Vascular Smooth Muscle Cells by Inhibiting the MAPK/NF-κB Pathway and Matrix Metalloproteinase Expressions

血管平滑肌 MAPK/ERK通路 基质金属蛋白酶 细胞生物学 生长因子 血小板源性生长因子受体 化学 信号转导 药理学 癌症研究 生物 平滑肌 生物化学 内分泌学 受体
作者
Chin‐Feng Hsuan,Yi-Ting Kuo,Tzu-Hsien Chang,Yaling Chen,Hsin-Ya Houng,Natasha C. Chang,Sabrina Chang,Chi‐Chang Chang,Jer‐Yiing Houng
出处
期刊:Journal of Medicinal Food [Mary Ann Liebert, Inc.]
卷期号:28 (9): 921-933 被引量:1
标识
DOI:10.1089/jmf.2024.k.0263
摘要

Vascular smooth muscle cells (VSMCs) are vital to the structure of blood vessel walls. Under abnormal vascular conditions, VSMCs undergo a phenotypic transformation, leading to enhanced cell proliferation, migration, and matrix synthesis. This contributes to the development of vascular diseases such as atherosclerosis, arteriosclerosis, and restenosis. During this process, platelet-derived growth factor (PDGF)-BB is a key inducer of the VSMC phenotypic transformation. Abelmoschus manihot (L.) Medic flower (AMf) is known for its rich nutritional value and traditional medicinal uses. Its extract has been clinically used to treat kidney diseases, but its impact on VSMCs has not been documented. This study explored the inhibitory effects of AMf ethanol extract (AME), hot water extract (AMW), and supercritical CO2 extract (AMS), and their five indicator components (rutin, quercetin, isoquercitrin, myricetin, and hyperoside) on PDGF-BB-stimulated proliferation and migration using a rat aortic smooth muscle cell (RASMC) model. Both AME and AMS showed a significant dose-dependent inhibition of PDGF-BB-induced RASMC proliferation and migration, with AME being more effective than AMS. In contrast, AMW had no effect. The five indicator compounds also showed excellent inhibitory effects. AME treatment effectively reduced the phosphorylation of JNK, ERK, p38, and NF-κB, and downregulated the expressions of the migration-promoting factors MMP-2 and MMP-9 in PDGF-BB-stimulated RASMCs. These findings suggest that AME protects VSMCs by regulating the phosphorylation of the MAPK/NF-κB pathway and suppressing MMP expression. Consequently, AME may help prevent or slow the progression of vascular diseases.
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