[Mechanism of elaidic acid-induced lipid accumulation in vascular smooth muscle cells].

卫生研究 Pub Date : 2025-07-01 DOI:10.19813/j.cnki.weishengyanjiu.2025.04.021

Chenyang Xiao, Shuang Song, Jiyong Yin, Xiaofang Jia, Huijun Wang, Shaofeng Wei, Aidong Liu

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引用次数: 0

Abstract

Objective: To investigate the molecular mechanisms underlying EA(elaidic acid)-induced lipid accumulation in VSMCs(vascular smooth muscle cells).

Methods: CCK-8 assay determined the effects of EA(0-2.8 mmol/L) on MOVAS(murine aortic vascular smooth muscle cells)to select experimental concentrations. Oil Red O staining combined with quantitative lipid droplet analysis was conducted to examine the effects of EA on intracellular lipid droplet accumulation. Intracellular total cholesterol(TC) and triglyceride(TG) levels were quantified spectrophotometrically to assess EA's effects on intracellular lipid levels. Western blot analyzed protein expression of PPARγ, LXRα, ABCA1, and ABCG1 to delineate EA's pro-foamogenic mechanism.

Results: EA dose-dependently suppressed MOVAS viability(P<0.01). EA-treated groups exhibited significant increases in lipid droplet area/number and TC/TG content versus controls(P<0.01). EA downregulated PPARγ and LXRα protein expression(P<0.05), subsequently suppressing downstream targets ABCA1 and ABCG1(P<0.05).

Conclusion: EA disrupts lipid metabolism in VSMCs by inhibiting the PPARγ-LXRα-ABCA1/ABCG1 signaling pathway, thereby inducing lipid accumulation and promoting foam cell formation.

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elaidic酸诱导血管平滑肌细胞脂质积累的机制

目的：探讨elaidic酸诱导血管平滑肌细胞脂质积累的分子机制。方法：采用CCK-8法测定EA（0 ~ 2.8 mmol/L）对小鼠主动脉血管平滑肌细胞（MOVAS）的影响，选择实验浓度。油红O染色结合定量脂滴分析，检测EA对细胞内脂滴积累的影响。用分光光度法定量测定细胞内总胆固醇（TC）和甘油三酯（TG）水平，以评估EA&apos对细胞内脂质水平的影响。Western blot分析PPARγ、LXRα、ABCA1和ABCG1的蛋白表达，探讨EA&apos的促泡沫机制。结果：EA剂量依赖性地抑制MOVAS活性（P<0.01）。与对照组相比，ea处理组脂滴面积/数量和TC/TG含量显著增加（P<0.01）。EA下调PPARγ和LXRα蛋白表达（P<0.05），随后抑制下游靶点ABCA1和ABCG1（P<0.05）。结论：EA通过抑制PPARγ-LXRα-ABCA1/ABCG1信号通路，破坏VSMCs脂质代谢，诱导脂质积累，促进泡沫细胞形成。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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卫生研究

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