Effects of soluble Klotho and Wnt/β-catenin signaling pathway in vascular calcification in chronic kidney disease model rats and the intervention of Shenyuan granules
Xinrong Zou,
Changjiang Wang,
Lan Wang,
Shenghua Huang,
Danfang Deng,
Lamei Lin,
Xiaoqin Wang
Affiliations
Xinrong Zou
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Changjiang Wang
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Lan Wang
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Shenghua Huang
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Danfang Deng
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Lamei Lin
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Xiaoqin Wang
Department of Nephrology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China
Objective This study aimed to investigate the effect of the soluble Klotho (sKlotho)/Wnt/β-catenin signaling pathway on vascular calcification in rat models of chronic kidney disease (CKD) and the intervention effect of Shenyuan granules.Methods Rats with 5/6 nephrectomy and high phosphorus feeding were used to establish the vascular calcification model. The rats were given gradient doses of Shenyuan granules aqueous solution and calcitriol solution by gavage for 8 weeks, which were divided into experimental group and positive control group.Results The 5/6 nephrectomy combined with high phosphorus feeding induced thoracic aortic calcification in rats. Shenyuan granules intervention increased the serum sKlotho level, inhibited the mRNA and protein expression of Wnt1, β-catenin, and Runx2 in the thoracic aorta, and alleviated thoracic aortic media calcification in rats.Conclusion Shenyuan granules may partially regulate the Wnt/β-catenin signaling pathway via serum sKl to interfere with the expression of Runx2, thereby improving vascular calcification in CKD.