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Glutamine’s protection against brain damage in septic rats via increased protein oxygen-N-acetylglucosamine modification

谷氨酰胺 烯醇化酶 免疫印迹 内分泌学 内科学 败血症 脑损伤 热休克蛋白70 谷氨酸受体 谷氨酰胺合成酶 H&E染色 化学 生物化学 热休克蛋白 医学 免疫组织化学 氨基酸 受体 基因
作者
Jin Wang,Xinjian Lu,Kang Zheng,Jing Liang
出处
期刊:Neuroreport [Ovid Technologies (Wolters Kluwer)]
卷期号:32 (3): 214-222 被引量:3
标识
DOI:10.1097/wnr.0000000000001582
摘要

This study aimed to observe the effect of glutamine (Gln) on brain damage in septic rats and explore its possible mechanism.Ninety-three Sprague-Dawley rats were randomly divided into five groups: sham operation group, sepsis group, Gln-treated group, quercetin/Gln-treated group, and alloxan/Gln-treated group. The rats in each group were continuously monitored for mean arterial pressure (MAP) and heart rate changes for 16 h. Neuroreflex scores were measured 24 h after surgery. The water content of the brain tissue was measured. Plasma neuron enolase and cysteine protease-3 were measured using the ELISA. The expression levels of heat shock protein 70 (HSP70) and oxygen-N-acetylglucosamine (O-GlcNAc) were determined by western blot analysis. Finally, the brain tissue was observed via hematoxylin and eosin staining.The brain tissue water content, plasma neuron enolase content, brain tissue cysteine protease-3 content, and nerve reflex score were significantly lower in the Gln-treated group than in the sepsis group (P < 0.05). At the same time, the pathological brain tissue damage in the Gln-treated group was also significantly reduced. It is worth noting that the expression of HSP70 and the protein O-GlcNAc modification levels in the Gln-treated group were significantly elevated than the levels in the sepsis group (P < 0.05), and reversed by pretreatment with the HSP and O-GlcNAc inhibitors quercetion and alloxan.Gln can attenuate brain damage in rats with sepsis, which may be associated with increased protein O-GlcNAc modification.

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