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首页> 外文期刊>Cell cycle >1,25(OH)(2)D-3 improves blood lipid metabolism, liver function, and atherosclerosis by constraining the TGF-beta/Smad signaling pathway in rats with hyperlipidemia
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1,25(OH)(2)D-3 improves blood lipid metabolism, liver function, and atherosclerosis by constraining the TGF-beta/Smad signaling pathway in rats with hyperlipidemia

机译：1,25（OH）（2）D-3通过在高脂血症大鼠中约束TGF-β/ Smad信号通路来改善血脂代谢，肝功能和动脉粥样硬化

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摘要

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-beta 1 siRNA. Whole blood viscosity, plasma viscosity, hematocrit, and erythrocyte aggregation index were detected, together with levels of biochemical indexes, 6-keto-PGF1 alpha, and TXB2 in serum. Levels of oxidative stress indexes and inflammatory factors in serum and liver tissues were determined. TGF-beta 1 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-1 beta, TNF-alpha, and increased HLP-induced decrease of HDL-C, apoAI, 6-keto-PGF1 alpha, SOD, GSH-Px, CAT, and T-AOC. TGF-beta 1 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-beta/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-beta/Smad signaling pathway in rats with HLP.
机译：已经报告了1,25（OH）（2）D-3在某些疾病中起作用。然而，它在高脂血症（HLP）中的作用仍然未知。本研究旨在探讨1,25（OH）（2）D-3对HLP大鼠的影响。通过高脂饮食喂养，灌注不同剂量的1,25-（OH）（2）D-3和注射TGF-β1siRNA的大鼠模型。检测到全血粘度，血浆粘度，血细胞比容和红细胞聚集指数，以及血清中生化指标，6-酮-PGF1α和TXB2的水平。确定了血清和肝组织中氧化应激指数和炎症因子的水平。检测到血清，肝组织和主动脉中的TGF-β1和Smad3表达。 1,25（OH）（2）D-3降低HLP诱导的全血粘度，红细胞聚集指数，血浆粘度和血细胞比容，TC，TG，LDL-C，APOB，ALT，AST，TXB2， MDA，IL-1β，TNF-α和增加的HLP诱导的HDL-C，Apoai，6-keto-PGF1α，SOD，GSH-PX，CAT和T-AOC降低。 TGF-β1和SMAD3在血清中，肝组织和1,25（OH）（2）D-3处理大鼠的主动脉减少。高1,25（OH）（2）D-3剂量并抑制TGF-β/ SMAD信号通路缓解了HLP大鼠的脂质代谢，肝功能和动脉粥样硬化损伤。我们的研究发现，通过约束用HLP大鼠TGF-β/ Smad信号通路，1,25（OH）（2）D-3通过约束TGF-β/ Smad信号通路来改善血脂代谢，肝功能和动脉粥样硬化损伤。

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