Inhibition of Homeobox D10 Alleviates Acute Kidney Injury by Upregulating PI3K/AKT Signaling Proteins

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology Pub Date : 2022-06-01 DOI:10.1155/2022/2955546

Siqi Liu, Hui-xin Sun, Jingjie Guo, Linlin Ma

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引用次数: 0

Abstract

Purpose. To observe the protective effect of homeobox D10 (HOXD10) on acute kidney injury (AKI) by regulating PI3K/AKT signaling pathway is the purpose of this study.Methods. 30 rats were randomly divided into three groups: blank control group, model group, and HOXD10 interference group. The kidney function indexes, HOXD10 protein expression, histopathological features, tubulointerstitial injury, and PI3K and AKT protein expression levels of the three groups were analyzed. Results. Compared with the blank control group, the kidney weight, BUN and SCr in model group increased significantly, and TIL score was higher ( P > 0.05 ). The expression of HOXD10 in model group and HOXD10 interference group were higher than blank control group, and the expression of HOXD10 in HOXD10 interference group was lower than model group ( P < 0.05 ). After we administered HOXD10 blocker to AKI rats, pathological sections by HE staining showed that the kidney tissue damage was significantly reduced compared with the model group, and the expression levels of BUN and SCr in kidney tissue decreased, and the TIL score decreased. The expression of p-PI3K and p-AKT decreased after kidney injury. Compared with the model group, the phosphorylation levels of PI3K and AKT in HOXD10 interference group were significantly increased ( P < 0.05 ). Conclusion. Downregulation of HOXD10 can play a protective role on AKI by activating PI3K/AKT signaling pathway, which can reduce tubulointerstitial injury and improve kidney function.

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同源盒D10抑制通过上调PI3K/AKT信号蛋白减轻急性肾损伤

目的。本研究旨在观察同源盒D10 (HOXD10)通过调控PI3K/AKT信号通路对急性肾损伤(AKI)的保护作用。30只大鼠随机分为3组:空白对照组、模型组、HOXD10干扰组。分析三组大鼠肾功能指标、HOXD10蛋白表达、组织病理学特征、肾小管间质损伤及PI3K、AKT蛋白表达水平。结果。与空白对照组比较，模型组大鼠肾重、BUN、SCr显著升高，TIL评分较高(P < 0.05)。模型组和HOXD10干扰组HOXD10表达均高于空白对照组，HOXD10干扰组HOXD10表达均低于模型组(P < 0.05)。给药后，HE染色病理切片显示，AKI大鼠肾组织损伤较模型组明显减轻，肾组织中BUN、SCr表达水平降低，TIL评分降低。肾损伤后p-PI3K、p-AKT表达降低。与模型组比较，HOXD10干扰组大鼠PI3K、AKT磷酸化水平显著升高(P < 0.05)。结论。下调HOXD10可通过激活PI3K/AKT信号通路，对AKI起到保护作用，减轻肾小管间质损伤，改善肾功能。

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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.