Sironi Chiara, Bodega Francesca, Zocchi Luciano, Porta Cristina
Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Facoltà di Medicina e Chirurgia, Università degli Studi di Milano, Via Mangiagalli 32, 20133 Milano, Italy.
Antioxidants (Basel). 2019 Jul 17;8(7):225. doi: 10.3390/antiox8070225.
We investigated the effects of creatine treatment on jejunal phenotypes in a rat model of oxidative stress induced by acidosis. In particular, the activities of some antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase), the level of lipid peroxidation, the expression of heat shock proteins (HSP70), and the expression of the major carriers of the cells (Na/K-ATPase, sodium-glucose Transporter 1-SGLT1, and glucose transporter 2-GLUT2) were measured under control and chronic acidosis conditions. Creatine did not affect the activity of antioxidant enzymes in either the control or acidosis groups, except for catalase, for which the activity was reduced in both conditions. Creatine did not change the lipid peroxidation level or HSP70 expression. Finally, creatine stimulated (Na/K)-ATPase expression under both control and chronic acidosis conditions. Chronic acidosis caused reductions in the expression levels of GLUT2 and SGLT1. GLUT2 reduction was abolished by creatine, while the presence of creatine did not induce any strengthening effect on the expression of SGLT1 in either the control or chronic acidosis groups. These results indicate that creatine has antioxidant properties that are realized through direct interaction of the molecule with reactive oxygen species. Moreover, the administration of creatine seems to determine a functional strengthening of the tissue, making it more resistant to acidosis.
我们在酸中毒诱导的氧化应激大鼠模型中研究了肌酸治疗对空肠表型的影响。具体而言,在对照和慢性酸中毒条件下,测量了一些抗氧化酶(超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶和谷胱甘肽还原酶)的活性、脂质过氧化水平、热休克蛋白(HSP70)的表达以及细胞主要载体(钠钾ATP酶、钠葡萄糖转运体1-SGLT1和葡萄糖转运体2-GLUT2)的表达。肌酸对对照组或酸中毒组的抗氧化酶活性均无影响,但过氧化氢酶除外,在两种条件下其活性均降低。肌酸未改变脂质过氧化水平或HSP70表达。最后,在对照和慢性酸中毒条件下,肌酸均刺激了钠钾ATP酶的表达。慢性酸中毒导致GLUT2和SGLT1表达水平降低。肌酸消除了GLUT2的降低,而在对照组或慢性酸中毒组中,肌酸的存在均未对SGLT1的表达产生任何增强作用。这些结果表明,肌酸具有抗氧化特性,可通过该分子与活性氧的直接相互作用来实现。此外,肌酸的给药似乎决定了组织的功能增强,使其对酸中毒更具抵抗力。