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本文引用的文献

1
Inhibitory effects of bee venom on Propionibacterium acnes-induced inflammatory skin disease in an animal model.蜂毒对动物模型中痤疮丙酸杆菌诱导的炎症性皮肤病的抑制作用。
Int J Mol Med. 2014 Nov;34(5):1341-8. doi: 10.3892/ijmm.2014.1933. Epub 2014 Sep 12.
2
Inflammatory processes in renal fibrosis.肾脏纤维化中的炎症过程。
Nat Rev Nephrol. 2014 Sep;10(9):493-503. doi: 10.1038/nrneph.2014.114. Epub 2014 Jul 1.
3
Suramin alleviates glomerular injury and inflammation in the remnant kidney.苏拉明可减轻残肾肾小球损伤和炎症。
PLoS One. 2012;7(4):e36194. doi: 10.1371/journal.pone.0036194. Epub 2012 Apr 27.
4
Genetic or pharmacologic blockade of EGFR inhibits renal fibrosis.基因或药理学阻断 EGFR 可抑制肾纤维化。
J Am Soc Nephrol. 2012 May;23(5):854-67. doi: 10.1681/ASN.2011050493. Epub 2012 Feb 23.
5
Cellular and molecular mechanisms of renal fibrosis.肾脏纤维化的细胞和分子机制。
Nat Rev Nephrol. 2011 Oct 18;7(12):684-96. doi: 10.1038/nrneph.2011.149.
6
Diverse roles of TGF-β/Smads in renal fibrosis and inflammation.TGF-β/Smads 在肾脏纤维化和炎症中的多种作用。
Int J Biol Sci. 2011;7(7):1056-67. doi: 10.7150/ijbs.7.1056. Epub 2011 Sep 2.
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Renal microenvironments and macrophage phenotypes determine progression or resolution of renal inflammation and fibrosis.肾脏微环境和巨噬细胞表型决定了肾脏炎症和纤维化的进展或消退。
Kidney Int. 2011 Nov;80(9):915-925. doi: 10.1038/ki.2011.217. Epub 2011 Aug 3.
8
The protective role of Smad7 in diabetic kidney disease: mechanism and therapeutic potential.Smad7 在糖尿病肾病中的保护作用:机制与治疗潜力。
Diabetes. 2011 Feb;60(2):590-601. doi: 10.2337/db10-0403. Epub 2010 Oct 27.
9
Bee venom inhibits hepatic fibrosis through suppression of pro-fibrogenic cytokine expression.蜂毒通过抑制促纤维化细胞因子表达抑制肝纤维化。
Am J Chin Med. 2010;38(5):921-35. doi: 10.1142/S0192415X10008354.
10
An integrative view on the role of TGF-beta in the progressive tubular deletion associated with chronic kidney disease.从整体上看 TGF-β 在与慢性肾病相关的进行性肾小管缺失中的作用。
Kidney Int. 2010 Jun;77(11):950-5. doi: 10.1038/ki.2010.88. Epub 2010 Mar 24.

天然毒素蜂毒对单侧输尿管梗阻动物模型的抗纤维化作用。

Anti-fibrotic effect of natural toxin bee venom on animal model of unilateral ureteral obstruction.

作者信息

An Hyun Jin, Kim Kyung Hyun, Lee Woo Ram, Kim Jung Yeon, Lee Sun Jae, Pak Sok Cheon, Han Sang Mi, Park Kwan Kyu

机构信息

Department of Pathology, College of Medicine, Catholic University of Daegu, 3056-6, Daemyung-4-Dong, Nam-gu, Daegu 705-718, Korea.

School of Biomedical Sciences, Charles Sturt University, Panorama Avenue, Bathurst, NSW 2795, Australia.

出版信息

Toxins (Basel). 2015 May 29;7(6):1917-28. doi: 10.3390/toxins7061917.

DOI:10.3390/toxins7061917
PMID:26035488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4488681/
Abstract

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.

摘要

进行性肾纤维化是所有导致慢性肾衰竭的肾脏疾病的最终共同途径。蜂毒(BV)已被广泛用作治疗各种疾病的传统药物。然而,BV改善肾纤维化的确切机制尚未完全明确。为了研究BV对单侧输尿管梗阻(UUO)诱导的肾纤维化的治疗作用,在输尿管结扎后腹腔注射BV。UUO手术后7天,收集肾脏组织进行蛋白质分析和组织学检查。组织学观察显示,UUO导致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,BV治疗显著减轻了这些反应。与UUO小鼠相比,BV治疗小鼠中TNF-α和IL-1β的表达水平显著降低。此外,BV治疗显著抑制了UUO小鼠中TGF-β1和纤连蛋白的表达。而且,BV治疗后α-SMA的表达明显下调。这些发现表明,BV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,BV可能是预防慢性肾病进展过程中特征性纤维化的有用治疗药物。

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