Anti-Fibrotic Effect of Natural Toxin Bee Venom on Animal Model of Unilateral Ureteral Obstruction

Toxins

Hyun Jin An¹  Kyung Hyun Kim¹  Woo Ram Lee¹  Jung Yeon Kim¹  Sun Jae Lee¹  Sok Cheon Pak³  Sang Mi Han²  Kwan Kyu Park¹ 

[1] Department of Pathology, College of Medicine, Catholic University of Daegu, 3056-6, Daemyung-4-Dong, Nam-gu, Daegu 705-718, Korea; E-Mails:;Department of Agricultural Biology, National Academy of Agricultural Science, RDA, 300, Nongsaengmyeong-ro, Wansan-gu, Jeonju-si, Jeollabuk-do 560-500, Korea; E-Mail:;School of Biomedical Sciences, Charles Sturt University, Panorama Avenue, Bathurst, NSW 2795, Australia; E-Mail:

关键词: bee venom;    renal fibrosis;    inflammation;    UUO;   

DOI  :  10.3390/toxins7061917

来源: mdpi

【 摘 要 】

Progressive renal fibrosis is the final common pathway for all kidney diseases leading to chronic renal failure. Bee venom (BV) has been widely used as a traditional medicine for various diseases. However, the precise mechanism of BV in ameliorating the renal fibrosis is not fully understood. To investigate the therapeutic effects of BV against unilateral ureteral obstruction (UUO)-induced renal fibrosis, BV was given intraperitoneally after ureteral ligation. At seven days after UUO surgery, the kidney tissues were collected for protein analysis and histologic examination. Histological observation revealed that UUO induced a considerable increase in the number of infiltrated inflammatory cells. However, BV treatment markedly reduced these reactions compared with untreated UUO mice. The expression levels of TNF-α and IL-1β were significantly reduced in BV treated mice compared with UUO mice. In addition, treatment with BV significantly inhibited TGF-β1 and fibronectin expression in UUO mice. Moreover, the expression of α-SMA was markedly withdrawn after treatment with BV. These findings suggest that BV attenuates renal fibrosis and reduces inflammatory responses by suppression of multiple growth factor-mediated pro-fibrotic genes. In conclusion, BV may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.