川芎嗪激活PPAR-γ通路并在血管钙化中发挥保护作用。
Ligustrazine activate the PPAR-γ pathway and play a protective role in vascular calcification.
作者信息
Li Hui, Yang Min
机构信息
Department of Cardiology, Shanxi Chinese Medical Hospital, Taiyuan, China.
Department of Medical Oncology, The Second Affiliate Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
出版信息
Vascular. 2022 Dec;30(6):1224-1231. doi: 10.1177/17085381211051477. Epub 2021 Oct 20.
OBJECTIVE
The purpose of this study was to explore the role of ligustrazine in vascular calcification.
METHODS
After β-GP stimulation, vascular smooth muscle cells (VSMCs) were detected by Alizarin Red Staing staining. Calcium content and alkaline phosphatase (ALP) activity were detected by intracellular calcium assay kit and ALP assay kit, respectively. The expression of peroxisome proliferation-activated receptor (PPAR-γ) pathway-related proteins was detected by Western blot. PPAR-γ, MSX2, osteopontin (OPN), sclerostin, and BGP were detected by RT-PCR.
RESULTS
β-GP induced the decreased activity and expression of PPAR-γ and ALP in VSMCs, while ligustrazine activated the expression of PPAR-γ. Through activation of PPAR-γ, ligustrazine decreased β-GP-induced VSMC calcification, decreased the expression of markers of osteogenesis and chondrogenic differentiation, and increased the expression of VSMC markers.
CONCLUSION
Ligustrazine activates the PPAR-γ pathway and plays a protective role in vascular calcification.
目的
本研究旨在探讨川芎嗪在血管钙化中的作用。
方法
经β-甘油磷酸（β-GP）刺激后，采用茜素红染色检测血管平滑肌细胞（VSMC）。分别用细胞内钙检测试剂盒和碱性磷酸酶（ALP）检测试剂盒检测钙含量和ALP活性。采用蛋白质免疫印迹法检测过氧化物酶体增殖物激活受体（PPAR-γ）途径相关蛋白的表达。采用逆转录-聚合酶链反应（RT-PCR）检测PPAR-γ、MSX2、骨桥蛋白（OPN）、硬化蛋白和骨钙素（BGP）。
结果
β-GP诱导VSMC中PPAR-γ活性及表达降低，同时降低ALP活性，而川芎嗪可激活PPAR-γ表达。通过激活PPAR-γ，川芎嗪可减轻β-GP诱导的VSMC钙化，降低成骨和软骨分化标志物的表达，并增加VSMC标志物的表达。
结论
川芎嗪激活PPAR-γ途径，对血管钙化起保护作用。
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