Xu Hao, Liu Guangyi, Gu Haitao, Wang Jijian, Li Yang
Master, Department of General Surgery, the People's Hospital of Kaizhou District, Chongqing, PR China. Conception and design of the study, analysis and interpretation of data, manuscript writing, final approval.
MD, Department of Gastrointestinal Surgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, PR China. Conception and design of the study, analysis and interpretation of data, manuscript writing, final approval.
Acta Cir Bras. 2020 Mar 9;35(1):e202000104. doi: 10.1590/s0102-865020200010000004. eCollection 2020.
Glutamine, as an essential part of enteral nutrition and parenteral nutrition agent, has been widely recognized to be a kind of important intestinal mucosa protectant in clinical practice and experimental research. However, the mechanisms of its protective effects are still not fully understand. Consequently, this study aimed to explore the potential mechanism of glutamine on ischemia-reperfusion (I/R) injury induced endoplasmic reticulum (ER) stress in intestine.
An experimental model of intestinal I/R in rats was established by 1 hour occlusion of the superior mesenteric artery followed by 3 hours of reperfusion. Morphologic changes of intestinal mucosa, apoptosis of epithelial cells, and expression of intestinal Grp78, Gadd153, Caspase-12, ATF4, PERK phosphorylation (P-PERK) and elF2αphosphorylation(P-elF2α) were determined.
After I/R, the apoptotic index of intestinal mucosa epithelial cells observably increased with notable necrosis of intestinal mucosa, and the expressions of Grp78, Gadd153, Caspase-12, ATF4, P-PERK and P-elF2αall were increased. However, treatment with glutamine could significantly relieve intestinal I/R injury and apoptosis index. Moreover, glutamine could clearly up-regulate the expression of Grp78, restrain P-PERK and P-elF2α, and reduce ATF4, Gadd153 and Caspase-12 expressions.
Glutamine may be involved in alleviating ER stress induced intestinal mucosa cells apoptosis.
谷氨酰胺作为肠内营养和肠外营养制剂的重要组成部分，在临床实践和实验研究中已被广泛认可为一种重要的肠黏膜保护剂。然而，其保护作用的机制仍未完全明确。因此，本研究旨在探讨谷氨酰胺对肠缺血再灌注（I/R）损伤诱导的内质网（ER）应激的潜在机制。
通过阻断大鼠肠系膜上动脉1小时，然后再灌注3小时，建立肠I/R实验模型。测定肠黏膜的形态学变化、上皮细胞凋亡以及肠组织中Grp78、Gadd153、Caspase-12、ATF4、PERK磷酸化（P-PERK）和elF2α磷酸化（P-elF2α）的表达。
I/R后，肠黏膜上皮细胞凋亡指数明显增加，肠黏膜出现明显坏死，Grp78、Gadd153、Caspase-12、ATF4、P-PERK和P-elF2α的表达均增加。然而，谷氨酰胺治疗可显著减轻肠I/R损伤和凋亡指数。此外，谷氨酰胺可明显上调Grp78的表达，抑制P-PERK和P-elF2α，并降低ATF4、Gadd153和Caspase-12的表达。
谷氨酰胺可能参与减轻内质网应激诱导的肠黏膜细胞凋亡。
