RETRACTED ARTICLE: 1,25(OH)₂D₃ improves blood lipid metabolism, liver function, and atherosclerosis by constraining the TGF-β/Smad signaling pathway in rats with hyperlipidemia

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, 6keto-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.

Exercise reduces hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient mice via its effects against inflammation and oxidative stress

“…The defense system of SOD and GSH-Px antioxidant enzymes is the first line of defense against oxidative injury in mammalian systems 19 , 20 . In this study, exercise was found to increase the SOD and GSH-Px levels, which is consistent with the findings of Lu et al 21 .…”

Insulin Resistance and Vitamin D Deficiency: A Link Beyond the Appearances

“…At a vascular level, the principal effect of vitamin D is an antioxidant action, by superoxide dismutase stimulation ( 22 ), counteracting the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, that promotes the synthesis of reactive oxygen species (ROS). As a consequence of its antioxidant action ( 42 , 43 ), vitamin D exerts beneficial effects on endothelial function ( 22 , 44 ), platelet aggregation ( 45 , 46 ), vascular inflammation ( 47 , 48 ), thrombogenesis ( 49 , 50 ), and vascular resistances and remodeling ( 51 – 53 ). Of note, vitamin D plays also a role in the regulation of angiogenesis and vascular repair by the synthesis of vascular endothelial growth factor (VEGF) and cell-derived factor 1 (SDF-1), respectively ( 54 , 55 ).…”

1,25(OH)2D3 inhibits Lewis lung cancer cell migration via NHE1‐sensitive metabolic reprograming

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