CD73 protects kidney from ischemia-reperfusion injury through reduction of free radicals
CD73 protects kidney from ischemia-reperfusion injury through reduction of free radicals
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CD73 通过减少自由基保护肾脏免受缺血再灌注损伤
DOI：
10.1111/j.1600-0463.2011.02827.x
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发表时间：
2012-02-01
期刊：
影响因子：
2.8
通讯作者：
Zhou, Ping
中科院分区：
文献类型：
--
作者：
Jian, Rongrong;Sun, Yong;Zhou, Ping
肾缺血再灌注损伤（IRI）可引起严重的全身性疾病。细胞外腺苷具有抗炎作用，特别是在低氧血症时。外5-核苷酸酶（CD73）是胞外腺苷生成的限速酶，它可能通过腺苷生成来保护肾IRI。在目前的研究中，我们研究了CD73在转基因小鼠中的作用。我们发现，与CD73 +/+小鼠相比，CD73-/-小鼠肾IRI引起更严重的组织损伤、血管通透性和脂质过氧化。此外，CD73-/-组AMP和自由基浓度明显高于CD73 +/+组。我们的数据支持这样一个事实，CD73可能通过腺苷的产生和自由基的减少来保护肾脏免受IRI。
Renal ischemia-reperfusion injury (IRI) may cause severe systemic diseases. Extracellular adenosine is anti-inflammatory especially during hypoxemia. As ecto-5-nucleotidase (CD73) is the rate-limiting enzyme for extracellular adenosine generation, it may protect renal IRI through adenosine production. In the current studies, we investigated the effects of CD73 in genetically modified mice. We found that renal IRI caused more serious histological injury, vascular permeability, and lipid peroxidation in CD73-/-) than that in CD73 +/+ mice. In addition, AMP and free radical concentrations were much higher in CD73-/-) than that in CD73 +/+ mice. Our data support the fact that CD73 may protect the kidney from IRI through adenosine production and a reduction of free radicals.