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氨酸防止细胞外超氧化物脱酶的表达和分泌减少,这种减少是由同类氨酸诱导的:通过氨酸缓解同类氨酸诱导的细胞内网膜应激

H Nonaka¹, T Tsujino, Y Watari

¹Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.

|September 6, 2001

概括

高水平的homocysteine会引起内细胞网膜 (ER) 的压力,减少细胞外超氧化物失调酶 (EC-SOD) 的分泌,促进动脉样硬化. 氨酸通过改善ER压力和恢复EC-SOD水平来抵消这种作用.

科学领域:

心血管生物学心血管生物学
细胞应激反应的应激反应
营养生物化学营养生物化学

背景情况:

超高囊血是动脉样硬化的一个已知的危险因素.
由未折叠的蛋白质积累而特征的内质网膜 (ER) 应激,与血管功能障碍有关.
氨酸通过需要阐明的机制表现出抗atherogenic 特性.

研究的目的:

调查同型半氨酸和氨酸对血管光滑肌细胞 (VSMCs) 细胞外超氧化解突变酶 (EC-SOD) 表达和分泌的影响.
阐明ER应激在同氨酸诱导的动脉样硬化中的作用和 taurine 的保护机制.

主要方法:

培养的老鼠VSMCs被用同型半氨酸和氨酸治疗.
基因表达 (EC-SOD,GRP78 mRNA) 使用北方斑点分析进行了评估.
蛋白质分泌 (EC-SOD) 通过西方斑点分析进行分析.
评估了ER压力标志物 (GRP78,PERK激活).

主要成果:

同类半氨酸显著降低了VSMC中的EC-SOD mRNA表达和蛋白质分泌.
同类氨酸诱导ER压力,由增加的GRP78mRNA和PERK激活证明.
氨酸有效地阻止了同类氨酸诱导的EC-SOD减少,并改善了ER压力.

结论:

类固醇因诱导ER压力而加剧动脉样硬化,这会损害VSMC中的EC-SOD分泌和表达,从而增加血管氧化应激.
氨酸通过改善ER压力来恢复EC-SOD水平,减轻 homocysteine 诱导的血管损伤.

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