Potential actions of capsaicin for preventing vascular calcification of vascular smooth muscle cells in vitro and in vivo
Yin-Fang Yan,
Yue Feng,
Si-Min Wang,
Fei Fang,
Hong-Yan Chen,
Ming-Xia Zhen,
Yu-Qiang Ji,
Song-Di Wu
Affiliations
Yin-Fang Yan
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Yue Feng
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Si-Min Wang
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Fei Fang
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Hong-Yan Chen
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Ming-Xia Zhen
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China
Yu-Qiang Ji
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China; Corresponding author: Department of central laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China.
Song-Di Wu
Department of Central Laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China; Xi'an Key Laboratory for Innovation and Translation of Neuroimmunological Diseases, Xi'an, Shaanxi Province, China; Corresponding author: Department of central laboratory, The First Affiliated Hospital of Northwestern University, The First Hospital of Xi'an, Xi'an, 710069, Shaanxi Province, China.
Vascular calcification (VC) is an accurate risk factor and predictor of adverse cardiovascular events; however, there is currently no effective therapy to specifically prevent VC progression. Capsaicin (Cap) is a bioactive alkaloid isolated from Capsicum annuum L., a traditional medicinal and edible plant that is beneficial for preventing cardiovascular diseases. However, the effect of Cap on VC remains unclear. This study aimed to explore the effects and related mechanisms of Cap on aortic calcification in a mouse and on Pi-induced calcification in vascular smooth muscle cells (VSMCs). First, we established a calcification mouse model with vitamin D3 and evaluated the effects of Cap on calcification mice using von Kossa staining, calcium content, and alkaline phosphatase activity tests. The results showed that Cap significantly improved calcification in mice. VSMCs were then cultured in 2.6 mM Na2HPO4 and 50 μg/mL ascorbic acid for 7 days to obtain a calcification model, and we investigated the effects and mechanisms of Cap on VSMCs calcification by assessing the changes of calcium deposition, calcium content, and subsequent VC biomarkers. These results showed that Cap alleviated VSMCs calcification by upregulating the expressions of TRPV1. Moreover, Cap reduced the expression of Wnt3a and β-catenin, whereas DKK1 antagonised the inhibitory effect of Cap on VSMC calcification. This study is the first to offer direct evidence that Cap inhibits the Wnt/β-catenin signaling pathway by upregulating the expression of the TRPV1 receptor, resulting in the decreased expression of Runx2 and BMP-2, thereby reducing VSMC calcification. Our study may provide novel strategies for preventing the progression of VC. This could serve as a theoretical basis for clinically treating VC with spicy foods.
