Glutamine protects intestinal calcium absorption against oxidative stress and apoptosis
Glutamine protects intestinal calcium absorption against oxidative stress and apoptosis
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DOI：
10.1016/j.cbpa.2017.07.006
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发表时间：
2017-10-01
影响因子：
2.3
通讯作者：
Tolosa de Talamoni, Nori
中科院分区：
文献类型：
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作者：
Moines, Luciana;Diaz de Barboza, Gabriela;Tolosa de Talamoni, Nori
本研究旨在探讨谷氨酰胺（GLN）是否能阻断甲萘醌（MEN）对小肠钙吸收的抑制作用，并探讨其作用机制。为此，将一个月大的雏鸡分成四组：1）对照组，2）MEN处理组，3）GLN处理组和4）在MEN处理之前或之后GLN处理组。肠钙吸收以及蛋白质表达的分子参与跨细胞钙通道进行了测定。测定了谷胱甘肽（GSH）、超氧阴离子（O2-）和抗氧化系统酶的活性。TUNEL法检测细胞凋亡、FAS、FASL表达及caspase-3活性。既往剂量为0.5 g GLN/kg b.w.为显示其保护作用，剂量为1 g/kg b.w.能恢复MEN治疗后肠道对Ca ~（2+）的吸收。GLN单独不改变钙结合蛋白D28 k和质膜Ca ~（2+）-ATP酶的蛋白表达，但阻断醌的抑制作用。GLN避免了由MEN引起的肠道氧化还原状态的变化，如GSH含量的减少，超氧阴离子和SOD和CAT活性的增加。GLN消除了MEN在肠粘膜中引起的凋亡效应，如TUNEL（+）细胞和FAS/FASL/caspase-3途径的减少所示。总之，GLN可以是一种口服营养补充剂，以使小肠中的氧化还原状态和增殖/细胞死亡比率正常化，从而改善由氧化应激改变的肠道Ca 2+吸收。
The aim of this study was to investigate whether glutamine (GLN) could block the inhibition of the intestinal Ca2+ absorption caused by menadione (MEN), and elucidate the underlying mechanisms. To do this, one-month old chicks were divided in four groups: 1) controls, 2) MEN treated, 3) GLN treated and 4) GLN treated before or after MEN treatment. Intestinal Ca2+ absorption as well as protein expression of molecules involved in the transcellular Ca2+ pathway were determined. Glutathione (GSH) and superoxide anion and activity of enzymes of the antioxidant system were evaluated. Apoptosis was measured by the TUNEL technique, the expression of FAS and FASL and the caspase-3 activity. A previous dose of 0.5 g GLN/kg of b.w. was necessary to show its protector effect and a dose of 1 g/kg of b.w. could restore the intestinal Ca2+ absorption after MEN treatment. GLN alone did not modify the protein expression of calbindin D28k and plasma membrane Ca2+-ATPase, but blocked the inhibitory effect of the quinone. GLN avoided changes in the intestinal redox state provoked by MEN such as a decrease in the GSH content, and increases in the superoxide anion and in the SOD and CAT activities. GLN abrogated apoptotic effects caused by MEN in intestinal mucosa, as indicated by the reduction of TUNEL (+) cells and the FAS/FASL/caspase-3 pathway. In conclusion, GLN could be an oral nutritional supplement to normalize the redox state and the proliferation/cell death ratio in the small intestine improving the intestinal Ca2+ absorption altered by oxidative stress.