Neuroprotective effect of glutamine supplementation by inhibiting oxidative stress and promoting autophagy responses after traumatic brain injury in rats

Q4 Nursing 中华临床营养杂志 Pub Date : 2019-04-30 DOI:10.3760/CMA.J.ISSN.1674-635X.2019.02.004

Shukai Wu, Xiangrong Chen, Yasong Li, L. Luo

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Abstract

Objective To investigate the effects and mechanisms of glutamine(Gln) supplementation on oxidative stress, autophagy response and neurobehavioral outcome after traumatic brain injury (TBI) in rats. Methods TBI animal models were established using Feeney's method. Eighty SD rats were randomly divided into 4 groups: sham operation group (group Sham), Sham + glutamine supplementation group (group Sham+ GLN), traumatic brain injury group (group TBI), and TBI + glutamine supplementation group (group TBI+ GLN). We measured rat behavioral outcomes by modified neurologic severity score (mNSS) tests at day 1, 3, 7 and 14 after TBI. The apoptosis neurons in TBI cerebral cortex were determined by TUNEL staining. The expression of reactive oxygen species (ROS) was tested by ROS kits. Oxidative stress and autophagy related cytokines (HO-1, NQO1, Nrf2, LC3-Ⅱ and Beclin-1) were tested with Western blotting. Results Compared with the TBI group, the neurological function was improved[(9.79±0.43)vs.(8.43±0.30), F=6.775, P=0.010] and the apoptosis rate decreased(19.88% ±1.60% vs. 15.35% ±1.28%, P=0.013) in the TBI+ GLN group after 7-day treatment. Compared with the Sham group, the protein expression of ROS increased(P=0.000), and the expression of anti-oxidative stress factors (HO-1, NQO1) and Nrf2 pathway significantly decreased in the TBI group. After glutamine supplementation was given, the expression of ROS decreased and the expressions of HO-1 and NQO1 increased. The Nrf2 pathway and autophagy response also were activated with the expressions of Nrf2, LC3-Ⅱ and Beclin-1 increasing. Conclusion Glutamine supplementation can markedly reduce neuron apoptosis and improve neurological outcomes after TBI, thus has the protective effect on nerves by inhibiting TBI-induced oxidative stress response, activating Nrf2 pathway and autophagy response. Key words: Traumatic brain injury; Glutamine; Oxidative stress; Nrf2 pathway; Autophagy

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谷氨酰胺补充对大鼠颅脑损伤后氧化应激和自噬反应的抑制作用

目的探讨谷氨酰胺（Gln）对大鼠创伤性脑损伤（TBI）后氧化应激、自噬反应和神经行为结果的影响及其机制。方法采用Feeney法建立TBI动物模型。80只SD大鼠随机分为4组：假手术组（sham组）、sham+谷氨酰胺补充组（sham+GLN组）、颅脑损伤组（TBI组）和TBI+谷氨酰胺补充小组（TBI+GLN）。我们在TBI后第1、3、7和14天通过改良神经严重程度评分（mNSS）测试来测量大鼠的行为结果。TUNEL染色法检测TBI大脑皮层细胞凋亡。活性氧试剂盒检测活性氧的表达。Western印迹法检测氧化应激和自噬相关细胞因子（HO-1、NQO1、Nrf2、LC3-Ⅱ和Beclin-1）。结果与TBI组相比，TBI+GLN组治疗7天后神经功能改善[（9.79±0.43）vs.（8.43±0.30），F=6.775，P=0.010]，细胞凋亡率下降[（19.88%±1.60%vs.15.35%±1.28%，P=0.013）。与Sham组相比，TBI组ROS的蛋白表达增加（P=0.000），抗氧化应激因子（HO-1，NQO1）和Nrf2通路的表达显著降低。补充谷氨酰胺后，ROS的表达减少，HO-1和NQO1的表达增加。Nrf2通路和自噬反应也随着Nrf2、LC3-Ⅱ和Beclin-1表达的增加而激活。结论补充谷氨酰胺可显著降低TBI后神经细胞凋亡，改善神经预后，通过抑制TBI诱导的氧化应激反应、激活Nrf2通路和自噬反应对神经具有保护作用。关键词：创伤性脑损伤；谷氨酰胺；氧化应激；Nrf2通路；自噬

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