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肾缺血再灌注导致心脏中硫化氢减少和氧化应激增加。

Kidney Ischemia-Reperfusion Decreases Hydrogen Sulfide and Increases Oxidative Stress in the Heart.

机构信息

St. Boniface Hospital Research Centre, Winnipeg, MB R2H 2A6, Canada.

Department of Animal Science, University of Manitoba, Winnipeg, MB R3T 2N2, Canada.

出版信息

Biomolecules. 2020 Nov 17;10(11):1565. doi: 10.3390/biom10111565.

DOI:10.3390/biom10111565
PMID:33212962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7698428/
Abstract

Patients with acute kidney injury (AKI) have an increased risk of cardiovascular disease. The underlying mechanism of AKI-induced heart injury is not well-understood. Hydrogen sulfide (HS), at physiological concentrations, has been implicated in cardiovascular protection through redox balance and vessel relaxation. Cystathionine gamma-lyase (CSE) plays an essential role in HS production in the heart. The present study investigated the effect of AKI on HS production and oxidative stress in the heart. AKI was induced by kidney ischemia-reperfusion in male and female Sprague-Dawley rats, which led to an increase in plasma creatinine and blood urea nitrogen levels. There was a significant increase in lipid peroxidation and a decrease in glutathione (antioxidant) levels in the plasma and heart, indicating systemic and cardiac oxidative stress. Kidney ischemia-reperfusion reduced CSE expression and HS production in the heart. There was a decrease in antioxidant transcription factor Nrf2 level in the nucleus and an increase in inflammatory cytokine (IL-6, TNF-α) expression in the heart. These results suggest that AKI can down-regulate CSE-mediated HS production, reduce glutathione levels and increase oxidative stress in the heart. This may contribute to an increased risk of cardiovascular disease in AKI.

摘要

急性肾损伤 (AKI) 患者发生心血管疾病的风险增加。AKI 导致心脏损伤的潜在机制尚不清楚。在生理浓度下，硫化氢 (HS) 通过氧化还原平衡和血管松弛来发挥心血管保护作用。胱硫醚 γ-裂解酶 (CSE) 在心脏 HS 的产生中发挥重要作用。本研究探讨了 AKI 对心脏 HS 产生和氧化应激的影响。通过雄性和雌性 Sprague-Dawley 大鼠的肾脏缺血再灌注来诱导 AKI，导致血浆肌酐和血尿素氮水平升高。血浆和心脏中的脂质过氧化明显增加，谷胱甘肽 (抗氧化剂) 水平降低，表明存在全身和心脏氧化应激。肾脏缺血再灌注降低了心脏中的 CSE 表达和 HS 产生。核中抗氧化转录因子 Nrf2 水平降低，心脏中炎症细胞因子 (IL-6、TNF-α) 的表达增加。这些结果表明，AKI 可以下调 CSE 介导的 HS 产生，降低谷胱甘肽水平并增加心脏中的氧化应激。这可能导致 AKI 患者发生心血管疾病的风险增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/3e10cd6abc8a/biomolecules-10-01565-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/4c2baffd64c8/biomolecules-10-01565-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/a29b05f56390/biomolecules-10-01565-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/33b43dc1ed7f/biomolecules-10-01565-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/782cc4bf700f/biomolecules-10-01565-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/a52f61ed86e0/biomolecules-10-01565-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/3e10cd6abc8a/biomolecules-10-01565-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/4c2baffd64c8/biomolecules-10-01565-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/a29b05f56390/biomolecules-10-01565-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/33b43dc1ed7f/biomolecules-10-01565-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/782cc4bf700f/biomolecules-10-01565-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/a52f61ed86e0/biomolecules-10-01565-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbfb/7698428/3e10cd6abc8a/biomolecules-10-01565-g006.jpg

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