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二甲双胍抑制多囊蛋白-2 缺陷斑马鱼模型中的囊肿形成。

Metformin Inhibits Cyst Formation in a Zebrafish Model of Polycystin-2 Deficiency.

机构信息

Kidney Research Center and Department of Nephrology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.

Graduate Institute of Biomedical Sciences, College of Medicine, Chang-Gung University, Taoyuan, Taiwan.

出版信息

Sci Rep. 2017 Aug 2;7(1):7161. doi: 10.1038/s41598-017-07300-x.

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a common kidney disease caused by mutations in PKD1 or PKD2. Metformin reduces cyst growth in mouse models of PKD1. However, metformin has not been studied in animal models of PKD2, and the cellular mechanism underlying its effectiveness is not entirely clear. This study investigated the effects of metformin on cyst formation in a zebrafish model of polycystin-2 deficiency resulting from morpholino knockdown of pkd2. We added metformin (2.5 to 20 mM) to the embryo media between 4 and 48 hours post fertilisation and observed pronephric cyst formation by using the wt1b promoter-driven GFP signal in Tg(wt1b:GFP) pkd2 morphants. Metformin inhibited pronephric cyst formation by 42-61% compared with the untreated controls. Metformin also reduced the number of proliferating cells in the pronephric ducts, the degree of dorsal body curvature, and the infiltration of leukocytes surrounding the pronephros. Moreover, metformin treatment increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and enhanced autophagy in the pronephros. Our data suggest that metformin reduces cyst formation through activation of the AMPK pathway and modulation of defective cellular events such as proliferation and autophagy. These results also imply that metformin could have therapeutic potential for ADPKD treatment.

摘要

常染色体显性多囊肾病(ADPKD)是一种常见的肾脏疾病,由 PKD1 或 PKD2 基因突变引起。二甲双胍可减少 PKD1 小鼠模型中的囊肿生长。然而,二甲双胍在 PKD2 动物模型中尚未得到研究,其有效性的细胞机制尚不完全清楚。本研究在多聚蛋白-2 缺陷的斑马鱼模型中,通过 PKD2 的 morpholino 敲低研究了二甲双胍对囊肿形成的影响。我们在受精后 4 至 48 小时将二甲双胍(2.5 至 20mM)添加到胚胎培养基中,并通过 Tg(wt1b:GFP)pkd2 morphants 的 wt1b 启动子驱动 GFP 信号观察前肾囊肿的形成。与未处理的对照组相比,二甲双胍抑制前肾囊肿形成 42-61%。二甲双胍还减少了前肾管中增殖细胞的数量、背部身体弯曲的程度以及围绕前肾的白细胞浸润。此外,二甲双胍处理增加了前肾中 AMPK 的磷酸化和自噬。我们的数据表明,二甲双胍通过激活 AMPK 途径和调节增殖和自噬等缺陷细胞事件来减少囊肿形成。这些结果还表明,二甲双胍可能对 ADPKD 的治疗具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4d3/5541071/0c4d8a75936e/41598_2017_7300_Fig1_HTML.jpg

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