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Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response
Oxidative Medicine and Cellular Longevity ( IF 7.310 ) Pub Date : 2020-11-11 , DOI: 10.1155/2020/8965047
Xiao-Hua Yu 1 , Jiao-Jiao Chen 1 , Wen-Yi Deng 1 , Xiao-Dan Xu 2 , Qi-Xian Liu 3 , Meng-Wen Shi 3 , Kun Ren 4
Affiliation  

Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE-/- mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) and PPARγ/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPARγ/LXRα and PPARγ/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.

中文翻译:

Biochanin A通过抑制脂质蓄积和炎症反应减轻动脉粥样硬化

从红三叶草和卷心菜中提取的一种膳食异黄酮生物chanin A(BCA)已被证明可拮抗高血压和心肌缺血/再灌注损伤。然而,对其在动脉粥样硬化中的作用了解甚少。这项研究的目的是观察BCA对动脉粥样硬化的影响并探讨其潜在机制。我们的结果表明,BCA的使用可促进胆固醇逆向转运(RCT),改善血脂水平并降低apoE -/-的血清促炎细胞因子水平和动脉粥样硬化病变区域老鼠喂了西餐。在THP-1巨噬细胞衍生的泡沫细胞中,BCA处理可通过激活过氧化物酶体增殖物激活受体γ(PPAR )上调ATP结合盒(ABC)转运蛋白A1(ABCA1)和ABCG1的表达,并促进随后的胆固醇外流并减少细胞内胆固醇的含量。γ)/肝X受体α(LXR α)和PPAR γ /血红素加氧酶1(HO-1)通路。BCA还激活了这两个信号通路,以抑制促炎细胞因子的分泌。总之,这些发现表明,BCA是动脉粥样硬化针对保护通过抑制通过PPAR脂质积聚和炎症反应γ / LXR α和PPAR γ / HO-1途径。BCA可能是预防和治疗动脉粥样硬化性心血管疾病的有吸引力的药物。
更新日期:2020-11-12
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