维生素D通过抗氧化、抗炎和AMPK/PI3K信号通路减轻大鼠代谢综合征诱导的肝损伤。

IF 3.2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2026-06-01 Epub Date: 2025-10-21 DOI:10.1080/13813455.2025.2573343

Suzan A Khodir, Eman M Sweed, Nahla M Badr, Nader G Zaki, Marwa M Khalil, Marwa M Adel

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引用次数: 0

摘要

背景：代谢综合征（MetS）涉及胰岛素抵抗和血脂异常。目的：探讨维生素D （Vit D）在MetS中的保肝作用及其机制。方法：30只雄性大鼠分为MetS组、MetS + Vit D组和对照组。我们测量了动脉血压（ABP）、体重、脂肪、胰岛素抵抗稳态模型评估（HOMA-IR）、血糖/脂质谱、肝酶、氧化应激（丙二醛、超氧化物歧化酶）、炎症（肿瘤坏死因子、TNF-α、基质金属蛋白酶、MMP9、胶质纤维酸性蛋白、GFAP）和amp活化的蛋白激酶/磷酸肌肽3激酶（AMPK/PI3K）的表达。结果：MetS增加氧化应激、TNF-α、肝酶、HOMA-IR和ABP，同时降低脂联素和AMPK/PI3K。维生素D逆转了这些作用，抑制GFAP/MMP9并恢复代谢平衡。结论：维生素D可通过激活AMPK/PI3K来减轻met诱导的肝损伤，发挥抗氧化和抗炎作用。

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Vit D mitigates metabolic syndrome-induced hepatic damage via antioxidant, anti-inflammatory, and AMPK/PI3K signaling pathways in rats.

Background: Metabolic syndrome (MetS) involves insulin resistance and dyslipidemia.

Objective: To evaluate vitamin D's (Vit D) hepatoprotective role in MetS and its mechanisms.

Methods: Thirty male rats were divided into MetS, MetS + Vit D, and control groups. We measured arterial blood pressure (ABP), body weight, fat, homeostatic Model Assessment for Insulin Resistance (HOMA-IR), glycemic/lipid profiles, liver enzymes, oxidative stress (Malondialdehyde, superoxide dismutase), inflammation (Tumor necrosis factor; TNF-α, matrix metalloproteinase; MMP9, Glial fibrillary acidic protein; GFAP), and AMP-activated protein kinase/Phosphoinositide 3-kinase (AMPK/PI3K) expression.

Results: MetS increased oxidative stress, TNF-α, liver enzymes, HOMA-IR, and ABP while reducing adiponectin and AMPK/PI3K. Vit D reversed these effects, suppressing GFAP/MMP9 and restoring metabolic balance. Conclusion: Vit D mitigates MetS-induced liver damage via AMPK/PI3K activation, exerting antioxidant and anti-inflammatory effects.

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.