Abstract

1,25(OH) 2 D 3 has already been reported to function in some diseases. However, its role in hyperlipidemia (HLP) remains unknown. This study aims to investigate the effect of 1,25(OH) 2 D 3 on HLP rats. Rat models were established by high-fat diet feeding, perfusion of different doses of 1,25-(OH) 2 D 3 and injection of TGF-β1 siRNA. Whole blood viscosity, plasma viscosity, hematocrit, and erythrocyte aggregation index were detected, together with levels of biochemical indexes, 6-keto-PGF1α, and TXB2 in serum. Levels of oxidative stress indexes and inflammatory factors in serum and liver tissues were determined. TGF-β1 and Smad3 expression in serum, liver tissues, and aorta was detected. 1,25(OH) 2 D 3 lowered HLP-induced rise of whole blood viscosity, red blood cell aggregation index, plasma viscosity, and hematocrit, TC, TG, LDL-C, apoB, ALT, AST, TXB2, MDA, IL-1β, TNF-α, and increased HLP-induced decrease of HDL-C, apoAI, 6-keto-PGF1α, SOD, GSH-Px, CAT, and T-AOC. TGF-β1 and Smad3 expression in serum, liver tissue, and aorta of 1,25(OH) 2 D 3 -treated rats reduced. High 1,25(OH) 2 D 3 dose and inhibited TGF-β/Smad signaling pathway alleviated lipid metabolism, liver function, and atherosclerotic injury in HLP rats. Our study found that 1,25(OH) 2 D 3 improves blood lipid metabolism, liver function, and atherosclerosis injury by constraining the TGF-β/Smad signaling pathway in rats with HLP.