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超氧化物歧化酶1缺失减轻了血管紧张素II输注下高血压小鼠的炎症性主动脉重塑。

Deletion of Superoxide Dismutase 1 Blunted Inflammatory Aortic Remodeling in Hypertensive Mice under Angiotensin II Infusion.

作者信息

Shiraishi Yasunaga, Ishigami Norio, Kujiraoka Takehiko, Sato Atsushi, Fujita Masanori, Ido Yasuo, Adachi Takeshi

机构信息

Division of Environmental Medicine, National Defense Medical College Research Institute, 3-2 Namiki, Tokorozawa Saitama 359-8513, Japan.

Department of Internal Medicine, Division of Cardiovascular Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa Saitama 359-8513, Japan.

出版信息

Antioxidants (Basel). 2021 Mar 16;10(3):471. doi: 10.3390/antiox10030471.

DOI:10.3390/antiox10030471
PMID:33809716
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8002308/
Abstract

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of two superoxide anions (O) into hydrogen peroxide (HO) and oxygen (O) and is generally known to protect against oxidative stress. Angiotensin II (AngII) causes vascular hypertrophic remodeling which is associated with HO generation. The aim of this study is to investigate the role of cytosolic SOD (SOD1) in AngII-induced vascular hypertrophy. We employed C57/BL6 mice (WT) and SOD1 deficient mice (SOD1) with the same background. They received a continuous infusion of saline or AngII (3.2 mg/kg/day) for seven days. The blood pressures were equally elevated at 1.5 times with AngII, however, vascular hypertrophy was blunted in SOD1 mice compared to WT mice (WT mice 91.9 ± 1.13 µm versus SOD1 mice 68.4 ± 1.41 µm < 0.001). The elevation of aortic interleukin 6 (IL-6) and phosphorylation of pro-inflammatory STAT3 due to AngII were also blunted in SOD1 mice's aortas. In cultured rat vascular smooth muscle cells (VSMCs), reducing expression of SOD1 with siRNA decreased AngII induced IL-6 release as well as phosphorylation of STAT3. Pre-incubation with polyethylene glycol (PEG)-catalase also attenuated phosphorylation of STAT3 due to AngII. These results indicate that SOD1 in VSMCs plays a role in vascular hypertrophy due to increased inflammation caused by AngII, probably via the production of cytosolic HO.

摘要

超氧化物歧化酶（SOD）是一种催化两个超氧阴离子（O）歧化为过氧化氢（HO）和氧气（O）的酶，通常被认为可抵御氧化应激。血管紧张素II（AngII）会导致与HO生成相关的血管肥厚性重塑。本研究的目的是探讨胞质超氧化物歧化酶（SOD1）在AngII诱导的血管肥厚中的作用。我们使用了具有相同背景的C57/BL6小鼠（野生型）和SOD1缺陷小鼠（SOD1）。它们连续七天接受生理盐水或AngII（3.2毫克/千克/天）输注。使用AngII后血压均升高至1.5倍，然而，与野生型小鼠相比，SOD1小鼠的血管肥厚受到抑制（野生型小鼠91.9±1.13微米，而SOD1小鼠68.4±1.41微米，<0.001）。SOD1小鼠主动脉中由于AngII导致的主动脉白细胞介素6（IL-6）升高和促炎信号转导和转录激活因子3（STAT3）磷酸化也受到抑制。在培养的大鼠血管平滑肌细胞（VSMC）中，用小干扰RNA（siRNA）降低SOD1的表达可减少AngII诱导的IL-6释放以及STAT3的磷酸化。用聚乙二醇（PEG）-过氧化氢酶预孵育也可减弱由于AngII导致的STAT3磷酸化。这些结果表明，VSMC中的SOD1可能通过产生胞质HO，在AngII引起的炎症增加所导致的血管肥厚中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/031d/8002308/3a17553e5df6/antioxidants-10-00471-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/031d/8002308/3a17553e5df6/antioxidants-10-00471-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/031d/8002308/1b19fdf22e05/antioxidants-10-00471-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/031d/8002308/71e258d83c75/antioxidants-10-00471-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/031d/8002308/79293f8183b4/antioxidants-10-00471-g003.jpg
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