芋媛 asked in 健康其他:保健 · 1 decade ago

會翻譯醫學的人快來幫幫我~

請問這是什麼意思?

Abstract

objectives:Experiments evaluated the hypothesis that angiotensin-converting enzyme(ACE) inhibition suppresses hyperglycemia-induced nitrotyrosine(NT)production in the renal cortex.

Design and methods: Rats were untreated(UNTR,n=6) or received the ACE inhibitor enalapril (20mg/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.

Results:Is the UNTR group,high glucose increased O2‾ and NOx production by the renal cortex(P<0.05 vs. normal glucose).Likewise,NT

content and SOD activity of the renal cortex augmedted(P<0.05 vs. normal glucose).In the ENAL group,O2‾ production and NT content were glucose-insensitive, but high glucose exerted an exagggerated impact on NOx production and SOD activity(P<0.01 vs. UNTR in high glucose).

Conclusio:Accelerated 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.

©2006 The Canadian Society of Clinical Chemists.All rights reserved.

Keywords:Diabetes mellitus;Angiotensin-converting enzyme inhibition;Superoxide anion;Nitric oxide;Peroxynitrite; Superoxide dismutase;Protein tyrosine nitration

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  • 1 decade ago
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    摘要

    目標:實驗評估假設,即血管緊張素轉換酶( ACE )抑制抑制高血糖引起的硝基酪氨酸( NT )的生產在腎皮質。

    設計與方法:大鼠未處理( untr ,每組6只) ,或收到了ACE抑製劑依那普利( 20mg/kg/day ; enal ,每組6只) , 2 weeks.renal皮質切片孵育90分鐘,在媒體載5 (正常)或20 mmol / L的(高)的葡萄糖,超氧陰離子( O2 〜 )和硝酸鹽+亞硝酸鹽( NOx )的水平來衡量,在media.superoxide氧化物歧化酶( SOD )活性和NT含量測定,在組織勻漿。

    結果:是untr組,高血糖增加氧氣〜和NOx生產由腎皮質性( P < 0.05正常血糖) ,同樣地,新台幣

    內容和超氧化物歧化酶活性的腎皮質augmedted性( P < 0.05正常血糖) ,在enal組,氧氣〜生產和NT含量分別為葡萄糖不敏感,但高血糖施加一個exagggerated影響NOx的生產和超氧化物歧化酶活性( P < 0.01 untr高糖) 。

    結論:加速新台幣含量在腎皮質,在高糖條件是阻止血管緊張素轉換酶抑製劑治療。有人認為,除了它的抗高血壓作用,其機制壓抑新台幣退化,在腎皮質由ACE抑製劑加強雙方氧氣〜退化本身的抗氧化作用,包括超氧化物歧化酶活性。

    © 2006年為加拿大社會的臨床chemists.all版權所有。

    關鍵詞:糖尿病;血管緊張素轉換酶抑製劑;超氧陰離子;一氧化氮;過氧超氧化物歧化酶蛋白酪氨酸硝化.

    Source(s): me
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