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高同型半胱氨酸血症加重顺铂诱导的急性肾损伤。

Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.

作者信息

Long Yanjun, Zhen Xin, Zhu Fengxin, Hu Zheng, Lei Wenjing, Li Shuang, Zha Yan, Nie Jing

机构信息

State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China;; Division of Nephrology, Guizhou Provincial People's Hospital, Guizhou Provincial Institute of Nephritic & Urinary Disease, Guiyang, P.R. China.

State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China.

出版信息

Int J Biol Sci. 2017 Feb 6;13(2):219-231. doi: 10.7150/ijbs.16725. eCollection 2017.

DOI:10.7150/ijbs.16725
PMID:28255274
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5332876/
Abstract

Hyperhomocysteinemia (HHcy) has been linked to several clinical manifestations including chronic kidney disease. However, it is not known whether HHcy has a role in the development of acute kidney injury (AKI). In the present study, we reported that HHcy mice developed more severe renal injury after cisplatin injection and ischemia-reperfusion injury shown as more severe renal tubular damage and higher serum creatinine. In response to cisplatin, HHcy mice showed more prevalent tubular cell apoptosis and decreased tubular cell proliferation. Mechanistically, a heightened ER stress and a reduced Akt activity were observed in kidney tissues of HHcy mice after cisplatin injection. Stimulating cultured NRK-52E cells with Hcy significantly increased the fraction of cells in G2/M phase and cell apoptosis together with decreased Akt kinase activity. Akt agonist IGF-1 rescued HHcy-induced cell cycle arrest and cell apoptosis. In conclusion, the present study provides evidence that HHcy increases the sensitivity and severity of AKI.

摘要

高同型半胱氨酸血症（HHcy）与包括慢性肾病在内的多种临床表现有关。然而，HHcy是否在急性肾损伤（AKI）的发生发展中起作用尚不清楚。在本研究中，我们报告称，HHcy小鼠在注射顺铂和经历缺血再灌注损伤后发生了更严重的肾损伤，表现为更严重的肾小管损伤和更高的血清肌酐水平。在对顺铂的反应中，HHcy小鼠表现出更普遍的肾小管细胞凋亡和肾小管细胞增殖减少。机制上，在注射顺铂后，HHcy小鼠的肾组织中观察到内质网应激增强和Akt活性降低。用同型半胱氨酸刺激培养的NRK-52E细胞可显著增加G2/M期细胞比例和细胞凋亡，同时降低Akt激酶活性。Akt激动剂IGF-1可挽救HHcy诱导的细胞周期阻滞和细胞凋亡。总之，本研究提供了证据表明HHcy会增加AKI的敏感性和严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b83/5332876/c2dbdfd188a3/ijbsv13p0219g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b83/5332876/c2dbdfd188a3/ijbsv13p0219g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b83/5332876/ad29ed990281/ijbsv13p0219g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b83/5332876/8dba726270d2/ijbsv13p0219g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b83/5332876/c2dbdfd188a3/ijbsv13p0219g007.jpg

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