Mauriz J L, Matilla B, Culebras J M, González P, González-Gallego J
Department of Physiology, University of León, León, Spain.
Free Radic Biol Med. 2001 Nov 15;31(10):1236-44. doi: 10.1016/s0891-5849(01)00716-x.
We investigated the effects of a glycine-containing diet (5%) on liver injury caused by hemorrhagic shock and resuscitation in rats. Anesthetized rats were bled to a mean arterial blood pressure of 35-40 mm Hg for 1 h and then resuscitated with 60% of shed blood and lactated Ringer's solution. Feeding the rats glycine significantly reduced mortality, the elevation of plasma transaminase levels and hepatic necrosis. The increase in plasma TNFalpha and nitric oxide (NO) was also blunted by glycine feeding. Hemorrhagic shock resulted in oxidative stress (significant elevations in TBARS and in the oxidized/reduced glutathione ratio) and was accompanied by a reduced activity of the antioxidant enzymes Mn- and Cu,Zn-superoxide dismutase, glutathione peroxidase and catalase, overexpression of inducible NO synthase (iNOS), and activation of nuclear factor kappa B (NF-kappaB). Glycine ameliorated oxidative stress and the impairment in antioxidant enzyme activities, inhibited NF-kappaB activation, and prevented expression of iNOS. Dietary glycine blocks activation of different mediators involved in the pathophysiology of liver injury after shock.
我们研究了含甘氨酸饮食（5%）对大鼠失血性休克及复苏所致肝损伤的影响。将麻醉的大鼠放血至平均动脉血压为35 - 40 mmHg，持续1小时，然后用60%的失血量和乳酸林格氏液进行复苏。给大鼠喂食甘氨酸可显著降低死亡率、血浆转氨酶水平的升高及肝坏死。喂食甘氨酸还可抑制血浆肿瘤坏死因子α（TNFα）和一氧化氮（NO）的增加。失血性休克导致氧化应激（丙二醛（TBARS）及氧化型/还原型谷胱甘肽比值显著升高），并伴有抗氧化酶锰超氧化物歧化酶、铜锌超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性降低，诱导型一氧化氮合酶（iNOS）过度表达以及核因子κB（NF - κB）激活。甘氨酸改善了氧化应激及抗氧化酶活性损伤，抑制了NF - κB激活，并阻止了iNOS表达。饮食中的甘氨酸可阻断休克后肝损伤病理生理过程中不同介质的激活。
