■苯并(a)芘(BaP),一种环境毒物和内分泌干扰物,已被证明与高脂肪饮食相结合会加剧动脉粥样硬化。成纤维细胞生长因子-21(FGF21),一种具有抗动脉粥样硬化特性的新型激素,与动脉粥样硬化的存在有关,并减少实验动物的斑块形成。
■本研究旨在探讨BaP注射液对肝脏FGF21表达的慢性影响,作为抗动脉粥样硬化激素,在有或没有动脉粥样硬化饮食(AtD)的小鼠中。
■根据剂量和饮食,将18只C57BL/6J雄性小鼠(6周)随机分为6组。采集血样,和血清胆固醇,甘油三酯,HDL-C,LDL-C,并测量葡萄糖水平。通过定量实时PCR评估FGF21表达。用油红O(ORO)染色研究小鼠的动脉粥样硬化病变。
■苯并(a)芘以剂量依赖性方式引起肝脏FGF21表达的显着增加,BaP与AtD共同暴露导致FGF21表达进一步增加。此外,在AtD中添加BaP显著增加了血清葡萄糖,胆固醇,和LDL-C水平,加速动脉粥样硬化病变的形成。此外,我们的研究结果表明,FGF21表达与葡萄糖之间存在显著正相关,胆固醇,LDL-C,和ORO积极的领域。
■我们的发现表明,BaP增加内源性FGF21在治疗动物中的表达,作为代偿性反应,保护心脏免受BaP和AtD诱导的动脉粥样硬化。
UNASSIGNED: Benzo(a)pyrene (BaP), an environmental toxicant and endocrine disruptor, has been shown to exacerbate atherosclerosis when combined with a high-fat diet. Fibroblast Growth Factor-21 (FGF21), a novel hormone with anti-atherosclerotic properties, is associated with the presence of atherosclerosis and reduces plaque formation in experimental animals.
UNASSIGNED: The present study aimed to investigate the chronic effect of BaP injection on hepatic FGF21 expression, as an anti-atherosclerotic hormone, in mice fed with or without an atherogenic diet (AtD).
UNASSIGNED: Eighteen C57BL/6J male mice (6 weeks) were randomly divided into six groups based on the dosage and diet. Blood samples were collected, and serum cholesterol, triglyceride, HDL-C, LDL-C, and glucose levels were measured. FGF21 expression was assessed by quantitative real-time PCR. Atherosclerotic lesions in mice were studied with Oil Red O (ORO) staining.
UNASSIGNED: Benzo(a)pyrene causes a significant increase in liver FGF21 expression in a dose-dependent manner, and BaP co-exposure with AtD leads to a further increase in FGF21 expression. Additionally, the addition of BaP to AtD significantly increased the serum glucose, cholesterol, and LDL-C levels and accelerated the formation of atherosclerotic lesions. Besides, our findings showed that there is a significant positive correlation between FGF21 expression and glucose, cholesterol, LDL-C, and ORO-positive areas.
UNASSIGNED: Our findings revealed that BaP increases the expression of endogenous FGF21 in treated animals as a compensatory response to protect the heart from atherosclerosis induced by BaP and AtD.