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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Ferulic Acid, an Angelica sinensis-Dcrived Polyphenol, Slows the Progression of Membranous Nephropathy in a Mouse Model
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Ferulic Acid, an Angelica sinensis-Dcrived Polyphenol, Slows the Progression of Membranous Nephropathy in a Mouse Model

机译:阿尔米亚酸,一只当归倒入的多酚,在小鼠模型中减慢膜状肾病的进展

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摘要

Membranous nephropathy (MN) is a leading cause of adult nephrotic syndrome but lacks adequate treatment. Different extracts of Angelica sinensis (AS) and one of its active compounds, ferulic acid (FA), were used to evaluate the therapeutic effects in a MN mouse model. The MN model was grouped into three subgroups: no treatment (N-T), treatment at induction of MN (Pre-T), and treatment after full-blown MN (Post-T). The results showed that the methanol (ME) layer of AS extract exhibited a therapeutic effect on MN-induced proteinuria. The ME layer-enriched compound, FA, improved the hypoalbuminemia, hyperlipidemia, and proteinuria in both Pre-T and Post-T groups. Ferulic acid also reduced the formation of oxidative protein products and increased the synthesis of antioxidant enzymes in groups Pre-T and Post-T. Regarding angiogenesis factors, the antiangiogenic factors in renal glomeruli were increased in group N-T, but, after FA treatment, only one of the antiangiogenic factors, thrombospondin-1, showed a significant decrease. Furthermore, the expression of Th2 predominant showed significant decrease in both Pre-T and Post-T groups when compared to that of N-T group. In summary, FA retarded the progression of MN, and the mechanisms involved the regulation of oxidative stresses, angiogenic and antiangiogenic factors, and attenuation of Th2 response.
机译:膜肾病(Mn)是成人肾病综合征的主要原因,但缺乏足够的治疗方法。 Angelica Sinensis(AS)的不同提取物和其活性化合物,阿魏酸(FA)的提取物用于评估Mn小鼠模型中的治疗效果。将Mn模型分为三个亚组:无治疗(N-T),在诱导Mn(Pre-T)的诱导中治疗,并在全吹动Mn(后T)后处理。结果表明,作为提取物的甲醇(ME)层表现出对MN诱导的蛋白尿的治疗作用。富含层的化合物,FA,改善了高血症血症,高脂血症和T型后T组。阿魏酸还降低了氧化蛋白质产物的形成,并增加了Th-T和后T组中抗氧化酶的合成。关于血管生成因子,N-T组肾肾小球中的抗血管生成因子增加,但是,在FA治疗后,只有一种抗血管生成因子,血压形素-1显示出显着降低。此外,与N-T组相比,Th2主导的表达显示出Pre-T和T组的显着降低。总之,FA延迟了Mn的进展,并且机制涉及调节氧化应激,血管生成和抗血管生成因子,以及TH2反应的衰减。

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