Impact of angiotensin-converting enzyme inhibition on renal cortical nitrotyrosine content during increased extracellular glucose concentration.
Impact of angiotensin-converting enzyme inhibition on renal cortical nitrotyrosine content during increased extracellular glucose concentration.
复制标题
细胞外葡萄糖浓度增加期间血管紧张素转换酶抑制对肾皮质硝基酪氨酸含量的影响。
DOI：
10.1016/j.clinbiochem.2006.02.005
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发表时间：
2006
影响因子：
2.8
通讯作者：
Katagiri,Masato
中科院分区：
文献类型：
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作者：
Ishii,Naohito;Ikenaga,Hideki;Carmines,PamelaK;Takada,Nobukazu;Okazaki,Toshio;Nagai,Tatsuo;Maeda,Tadakazu;Aoki,Yoshikazu;Saruta,Takao;Katagiri,Masato
目的实验评估了血管紧张素转换酶 (ACE) 抑制可抑制肾皮质中高血糖诱导的硝基酪氨酸 (NT) 产生的假设。设计和方法大鼠未经治疗（UNTR，n = 6）或接受 ACE 抑制剂依那普利（20 mg/kg/天；ENAL，n = 6）治疗 2 周。肾皮质切片在含有 5（正常）或 20 mmol/L（高）葡萄糖的培养基中孵育 90 分钟。测量介质中的超氧阴离子 (O2·−) 和硝酸盐 + 亚硝酸盐 (NOX) 水平。测量组织匀浆中的超氧化物歧化酶 (SOD) 活性和 NT 含量。 结果在 UNTR 组中，高葡萄糖增加肾皮质 O2·− 和 NOX 的产生（与正常葡萄糖相比，P < 0.05）。同样，肾皮质的 NT 含量和 SOD 活性也增加（与正常葡萄糖相比，P < 0.05）。在 ENAL 组中，O2·−产生和 NT 含量对葡萄糖不敏感，但高葡萄糖对 NOX 产生和 SOD 活性产生了夸大的影响（与高葡萄糖条件下的 UNTR 相比，P < 0.01）。结论 ACE 抑制剂治疗可防止高葡萄糖条件下肾皮质中 NT 含量的加速。有人提出，除了其抗高血压作用外，ACE抑制剂抑制肾皮质中NT降解的机制增强了O2·−降解本身和包括SOD活化在内的抗氧化作用。
OBJECTIVESExperiments evaluated the hypothesis that angiotensin-converting enzyme (ACE) inhibition suppresses hyperglycemia-induced nitrotyrosine (NT) production in the renal cortex.DESIGN AND METHODSRats were untreated (UNTR, n = 6) or received the ACE inhibitor enalapril (20 mg/kg/day; ENAL, n = 6) for 2 weeks. Renal cortical slices were incubated for 90 min in media containing 5 (normal) or 20 mmol/L (high) glucose. Superoxide anion (O2·−) and nitrate + nitrite (NOX) levels were measured in the media. Superoxide dismutase (SOD) activity and NT content were measured in the tissue homogenate.RESULTSIn the UNTR group, high glucose increased O2·−and NOXproduction by the renal cortex (P < 0.05 vs. normal glucose). Likewise, NT content and SOD activity of the renal cortex augmented (P < 0.05 vs. normal glucose). In the ENAL group, O2·−production and NT content were glucose-insensitive, but high glucose exerted an exaggerated impact on NOXproduction and SOD activity (P < 0.01 vs. UNTR in high glucose).CONCLUSIONAccelerated NT content in the renal cortex during high-glucose conditions was prevented by ACE inhibitor treatment. It was suggested that, apart from its anti-hypertensive effect, the mechanism of suppressed NT degradation in the renal cortex by the ACE inhibitor enhances both O2·−degradation per se and antioxidative effects including SOD activation.