{"title":"elaidic酸诱导血管平滑肌细胞脂质积累的机制","authors":"Chenyang Xiao, Shuang Song, Jiyong Yin, Xiaofang Jia, Huijun Wang, Shaofeng Wei, Aidong Liu","doi":"10.19813/j.cnki.weishengyanjiu.2025.04.021","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the molecular mechanisms underlying EA(elaidic acid)-induced lipid accumulation in VSMCs(vascular smooth muscle cells).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>EA disrupts lipid metabolism in VSMCs by inhibiting the PPARγ-LXRα-ABCA1/ABCG1 signaling pathway, thereby inducing lipid accumulation and promoting foam cell formation.</p>","PeriodicalId":57744,"journal":{"name":"卫生研究","volume":"54 4","pages":"681-687"},"PeriodicalIF":0.0000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Mechanism of elaidic acid-induced lipid accumulation in vascular smooth muscle cells].\",\"authors\":\"Chenyang Xiao, Shuang Song, Jiyong Yin, Xiaofang Jia, Huijun Wang, Shaofeng Wei, Aidong Liu\",\"doi\":\"10.19813/j.cnki.weishengyanjiu.2025.04.021\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the molecular mechanisms underlying EA(elaidic acid)-induced lipid accumulation in VSMCs(vascular smooth muscle cells).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>EA disrupts lipid metabolism in VSMCs by inhibiting the PPARγ-LXRα-ABCA1/ABCG1 signaling pathway, thereby inducing lipid accumulation and promoting foam cell formation.</p>\",\"PeriodicalId\":57744,\"journal\":{\"name\":\"卫生研究\",\"volume\":\"54 4\",\"pages\":\"681-687\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"卫生研究\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.19813/j.cnki.weishengyanjiu.2025.04.021\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"卫生研究","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.19813/j.cnki.weishengyanjiu.2025.04.021","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[Mechanism of elaidic acid-induced lipid accumulation in vascular smooth muscle cells].
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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