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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 5180165, 13 pages
Research Article

Herba Artemisiae Capillaris Extract Prevents the Development of Streptozotocin-Induced Diabetic Nephropathy of Rat

1Institute of Virology and AIDS, The First Hospital of Jilin University, Jilin University, Dongminzhu Street 519, Changchun 130000, China
2Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Fujin Road 1266, Changchun 130021, China
3Acupuncture Department, The Affiliated Hospital to Changchun University of Chinese Medicine, 1478 Gongnong Road, Changchun 130021, China
4Department of Pharmacology, College of Basic Medical Science, Jilin University, Xinmin Street 126, Changchun 130021, China
5Department of Obstetrics Gynecology, The Second Hospital of Jilin University, Ziqiang Street 218, Changchun 130041, China

Correspondence should be addressed to Yinggang Zou; nc.ude.ulj@gyuoz and Jinghua Yu; moc.361@2002-0-hjy

Received 18 August 2017; Revised 1 December 2017; Accepted 26 December 2017; Published 14 February 2018

Academic Editor: Youn C. Kim

Copyright © 2018 Jianan Geng 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.


Diabetic nephropathy (DN) is a major cause of end-stage renal disease throughout the world; until now there is no specific drug available. In this work, we use herba artemisiae capillaris extract (HACE) to alleviate renal fibrosis characterized by the excessive accumulation of extracellular matrix (ECM) in rats, aiming to investigate the protective effect of the HACE on DN. We found that the intragastric treatment of high-dose HACE could reverse the effect of streptozotocin not only to decrease the level of blood glucose and blood lipid in different degree but also further to improve renal functions. It is worth mentioning that the effect of HACE treatment was comparable to the positive drug benazepril. Moreover, we found that HACE treatment could on one hand inhibit oxidative stress in DN rats through regulating enzymatic activity for scavenging reactive oxygen species and on the other hand increase the ECM degradation through regulating the activity of metalloproteinase-2 (MMP-2) and the expression of tissue transglutaminase (tTG), which explained why HACE treatment inhibited ECM accumulation. On the basis of above experimental results, we conclude that HACE prevents DN development in a streptozotocin-induced DN rat model, and HACE is a promising candidate to cure DN in clinic.