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:阿魏酸,当归切碎的多酚,在小鼠模型中减慢膜性肾病的进展。

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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:膜性肾病(MN)是成人肾病综合征的主要原因,但缺乏适当的治疗。当归(AS)及其活性化合物之一阿魏酸(FA)的不同提取物用于评估MN小鼠模型的治疗效果。 MN模型分为三个子组:不治疗(N-T),诱导MN的治疗(Pre-T)和成年MN后的治疗(Post-T)。结果表明,AS提取物的甲醇层对MN诱导的蛋白尿有治疗作用。富含ME层的化合物FA可以改善Pre-T和Post-T组的低白蛋白血症,高脂血症和蛋白尿。阿魏酸还减少了Pre-T和Post-T组中氧化蛋白产物的形成并增加了抗氧化酶的合成。关于血管生成因子,N-T组肾小球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thrombospondin-1显着降低。此外,与N-T组相比,Pre-T组和Post-T组中Th2优势表达显着降低。总之,FA阻碍了MN的发展,其机制涉及氧化应激,血管生成和抗血管生成因子的调节以及Th2反应的减弱。

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