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Protective effects of melittin on renal fibrosis in an animal model of unilateral ureteral obstruction
Kwan-Kyu Park, MD, PhD, Hyun-Jin An, PhD, Woon-Hae Kim, MSc, Mi-Gyeong Gwon, BSc, Hyemin Gu, BSc, Minji Jeon, BSc, Hyun Chung, MD,PhD.
College of medicine, Catholic university of Daegu, Daegu, Korea, Republic of.

Background: Renal fibrosis is the principal pathological process underlying the progression of chronic kidney disease that leads to end-stage renal disease. Renal fibrosis is characterized by the infiltration of inflammatory cell, interstitial fibroblasts accumulation, proliferation of myofibroblasts, deposition of the extracellular matrix, and loss of renal tubule epithelial cells, which collectively lead to end-stage renal failure. Melittin is a major component of bee venom, and it has anti-bacterial, anti-viral, and anti-inflammatory properties in various cell types. Many studies have examined the biological and pharmacological activities of melittin. However, the precise mechanism of melittin in ameliorating the renal fibrosis is not fully understood. Therefore, this study examined the therapeutic effects of melittin on the progression of renal fibrosis using the unilateral ureteral obstruction (UUO) animal model. Furthermore, the effects of melittin on inflammation and fibrosis in renal fibroblast cells were explored using TGF-β1. Materials & methods: To investigate the therapeutic effects of melittin against unilateral UUO-induced renal fibrosis, melittin was given intraperitoneally after ureteral ligation. At seven days after UUO surgery, the kidney tissues were collected for protein analysis and histologic examination. Results: Histological observation revealed that UUO induced a considerable increase in the number of infiltrated inflammatory cells. However, melittin treatment markedly reduced these reactions compared with untreated UUO mice. The expression protein levels of TNF-α and IL-1β were significantly reduced in melittin treated mice compared with UUO mice. In addition, treatment with melittin significantly inhibited TGF-β1 and fibronectin expression in UUO mice. Immunofluorescence staining shows that melittin treatment reduces α-SMA-positive cells in the kidneys after UUO. Besides, melittin effectively inhibited fibrosis-related gene expression in renal fibroblasts NRK-49F cells. Conclusions: These findings suggest that melttin attenuates renal fibrosis and reduces inflammatory responses by suppression of multiple growth factor-mediated pro-fibrotic genes. In conclusion, melittin may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.


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