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蜂毒肽对单侧输尿管梗阻动物模型肾纤维化的保护作用

The Protective Effect of Melittin on Renal Fibrosis in an Animal Model of Unilateral Ureteral Obstruction.

作者信息

An Hyun-Jin, Kim Jung-Yeon, Kim Woon-Hae, Han Sang-Mi, Park Kwan-Kyu

机构信息

Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Korea.

Deparment of Agricultural Biology, National Academy of Agricultural Science, RDA, 300, Nongsaengmyeong-ro, Wansan-gu, Jeonju 54875, Korea.

出版信息

Molecules. 2016 Aug 27;21(9):1137. doi: 10.3390/molecules21091137.

DOI:10.3390/molecules21091137
PMID:27618890
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6274242/
Abstract

Renal fibrosis is the principal pathological process underlying the progression of chronic kidney disease that leads to end-stage renal disease. Melittin is a major component of bee venom, and it has anti-bacterial, anti-viral, and anti-inflammatory properties in various cell types. Thus, this study examined the therapeutic effects of melittin on the progression of renal fibrosis using the unilateral ureteral obstruction (UUO) model. In addition, the effects of melittin on inflammation and fibrosis in renal fibroblast cells were explored using transforming growth factor-β1 (TGF-β1). 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 levels of inflammatory cytokines and pro-fibrotic genes were significantly reduced in melittin-treated mice compared with UUO mice. Melittin also effectively inhibited fibrosis-related gene expression in renal fibroblasts NRK-49F cells. These findings suggest that melittin attenuates renal fibrosis and reduces inflammatory responses by the 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 the progression of chronic kidney disease.

摘要

肾纤维化是导致终末期肾病的慢性肾脏病进展的主要病理过程。蜂毒肽是蜂毒的主要成分,在多种细胞类型中具有抗菌、抗病毒和抗炎特性。因此,本研究使用单侧输尿管梗阻(UUO)模型研究了蜂毒肽对肾纤维化进展的治疗作用。此外,使用转化生长因子-β1(TGF-β1)探讨了蜂毒肽对肾成纤维细胞炎症和纤维化的影响。组织学观察显示,UUO诱导浸润性炎症细胞数量显著增加。然而,与未治疗的UUO小鼠相比,蜂毒肽治疗显著减轻了这些反应。与UUO小鼠相比,蜂毒肽治疗的小鼠炎症细胞因子和促纤维化基因的表达水平显著降低。蜂毒肽还有效抑制了肾成纤维细胞NRK-49F细胞中与纤维化相关的基因表达。这些发现表明,蜂毒肽通过抑制多种生长因子介导的促纤维化基因来减轻肾纤维化并减少炎症反应。总之,蜂毒肽可能是预防慢性肾脏病进展过程中特征性纤维化的一种有用治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/ceb143f40e52/molecules-21-01137-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/ddac7aaed0a8/molecules-21-01137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/5657cc5172b1/molecules-21-01137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/3fffd5e382b7/molecules-21-01137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/ceb143f40e52/molecules-21-01137-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/ddac7aaed0a8/molecules-21-01137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/5657cc5172b1/molecules-21-01137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/3fffd5e382b7/molecules-21-01137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbdc/6274242/ceb143f40e52/molecules-21-01137-g004.jpg

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