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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 161235, 12 pages
Research Article

Ferulic Acid, an Angelica sinensis-Derived Polyphenol, Slows the Progression of Membranous Nephropathy in a Mouse Model

1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250 Wu-Hsing Street, Xinyi District, Taipei City 110, Taiwan
2School of Pharmacy, National Defense Medical Center, No. 161, Section 6, Minquan E. Road, Neihu District, Taipei City 114, Taiwan
3Division of Nephrology, Department of Internal Medicine, Tri-Service General Hospital, No. 325, Section 2, Chenggong Road, Neihu District, Taipei City 114, Taiwan
4Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, No. 291, Zhongzheng Road, Zhonghe District, New Taipei City 235, Taiwan

Received 12 March 2012; Revised 14 May 2012; Accepted 14 May 2012

Academic Editor: Jairo Kenupp Bastos

Copyright © 2012 Chao-Wen Cheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.