苯恶洛芬通过明显调节蛋白激酶C来激活人多形核白细胞中与膜相关的氧化代谢。
Benoxaprofen activates membrane-associated oxidative metabolism in human polymorphonuclear leucocytes by apparent modulation of protein kinase C.
作者信息
Lukey P T, Anderson R, Dippenaar U H
机构信息
Department of Medical Microbiology, University of Pretoria, Republic of South Africa.
出版信息
Br J Pharmacol. 1988 Feb;93(2):289-94. doi: 10.1111/j.1476-5381.1988.tb11433.x.
Abstract
- The non-steroidal anti-inflammatory drug (NSAID) benoxaprofen at concentrations of 15, 30 and 60 micrograms ml-1 caused a dose-related activation of superoxide generation by human polymorphonuclear leucocytes (PMNL) in vitro. 2. The protein kinase C (PKC) inhibitor H-7 prevented benoxaprofen-mediated activation of superoxide generation by PMNL. 3. Benoxaprofen, by apparent substitution for phosphatidylserine, caused a dose-related activation of purified PKC from rat brain and in cytosolic extracts from human platelets. 4. Benoxaprofen-mediated stimulation of PMNL membrane-associated oxidative metabolism is due to apparent activation of PKC by this NSAID. These findings establish the molecular basis of the pro-oxidative properties of benoxaprofen.
摘要
- 非甾体抗炎药（NSAID）苯恶洛芬在浓度为15、30和60微克/毫升时，可在体外引起人多形核白细胞（PMNL）超氧化物生成的剂量相关性激活。2. 蛋白激酶C（PKC）抑制剂H-7可阻止苯恶洛芬介导的PMNL超氧化物生成激活。3. 苯恶洛芬通过明显替代磷脂酰丝氨酸，引起大鼠脑纯化PKC以及人血小板胞质提取物的剂量相关性激活。4. 苯恶洛芬介导的PMNL膜相关氧化代谢刺激是由于该NSAID对PKC的明显激活。这些发现确立了苯恶洛芬促氧化特性的分子基础。
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