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大鼠容量超负荷致充血性心力衰竭后肾脏的组织病理学变化

Histopathological Changes in the Kidney following Congestive Heart Failure by Volume Overload in Rats.

作者信息

Aboryag Noureddin B, Mohamed Doaa M, Dehe Lukas, Shaqura Mohammed, Treskatsch Sacha, Shakibaei Mehdi, Schäfer Michael, Mousa Shaaban A

机构信息

Department of Anaesthesiology and Intensive Care Medicine, Charité University Berlin, Campus Virchow Klinikum and Campus Charité Mitte, Berlin, Germany.

Department of Anatomy, Ludwig-Maximilians-University Munich, Munich, Germany.

出版信息

Oxid Med Cell Longev. 2017;2017:6894040. doi: 10.1155/2017/6894040. Epub 2017 Jul 31.

DOI:10.1155/2017/6894040
PMID:28831296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5555028/
Abstract

BACKGROUND

This study investigated histopathological changes and apoptotic factors that may be involved in the renal damage caused by congestive heart failure in a rat model of infrarenal aortocaval fistula (ACF).

METHODS

Heart failure was induced using a modified approach of ACF in male Wistar rats. Sham-operated controls and ACF rats were characterized by their morphometric and hemodynamic parameters and investigated for their histopathological, ultrastructural, and apoptotic factor changes in the kidney.

RESULTS

ACF-induced heart failure is associated with histopathological signs of congestion and glomerular and tubular atrophy, as well as nuclear and cellular degeneration in the kidney. In parallel, overexpression of proapoptotic Bax protein, release of cytochrome C from the outer mitochondrial membrane into cell cytoplasm, and nuclear transfer of activated caspase 3 indicate apoptotic events. This was confirmed by electron microscopic findings of apoptotic signs in the kidney such as swollen mitochondria and degenerated nuclei in renal tubular cells.

CONCLUSIONS

This study provides morphological evidence of renal injury during heart failure which may be due to caspase-mediated apoptosis via overexpression of proapoptotic Bax protein, subsequent mitochondrial cytochrome C release, and final nuclear transfer of activated caspase 3, supporting the notion of a cardiorenal syndrome.

摘要

背景

本研究在肾下主动脉腔静脉瘘（ACF）大鼠模型中，调查了可能参与充血性心力衰竭所致肾损伤的组织病理学变化和凋亡因子。

方法

采用改良的ACF方法诱导雄性Wistar大鼠发生心力衰竭。通过形态计量学和血流动力学参数对假手术对照组和ACF大鼠进行表征，并研究其肾脏的组织病理学、超微结构和凋亡因子变化。

结果

ACF诱导的心力衰竭与肾脏充血、肾小球和肾小管萎缩的组织病理学征象以及核与细胞变性有关。同时，促凋亡Bax蛋白的过表达、细胞色素C从线粒体外膜释放到细胞质以及活化的半胱天冬酶3的核转移表明发生了凋亡事件。肾脏中出现凋亡征象的电子显微镜检查结果证实了这一点，如肾小管细胞中的线粒体肿胀和细胞核变性。

结论

本研究提供了心力衰竭期间肾损伤的形态学证据，这可能是由于促凋亡Bax蛋白过表达、随后线粒体细胞色素C释放以及活化的半胱天冬酶3最终核转移导致的半胱天冬酶介导的凋亡，支持了心肾综合征的概念。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/0237046cd356/OMCL2017-6894040.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/03c367ea1e7c/OMCL2017-6894040.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/8ec481c009ea/OMCL2017-6894040.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/553c06a446c6/OMCL2017-6894040.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/57c02603cbf3/OMCL2017-6894040.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/c9a12bc6ba76/OMCL2017-6894040.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/f47b909bba81/OMCL2017-6894040.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/0237046cd356/OMCL2017-6894040.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/03c367ea1e7c/OMCL2017-6894040.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/8ec481c009ea/OMCL2017-6894040.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/553c06a446c6/OMCL2017-6894040.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/57c02603cbf3/OMCL2017-6894040.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/c9a12bc6ba76/OMCL2017-6894040.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/f47b909bba81/OMCL2017-6894040.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc38/5555028/0237046cd356/OMCL2017-6894040.007.jpg

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