Chen G, Shi J, Qi M, Yin H, Hang C
Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, PR China.
Inflamm Res. 2008 Feb;57(2):57-64. doi: 10.1007/s00011-007-7101-7.
To investigate whether glutamine supplementation modulates intestinal nuclear factor kappa B (NF-kappaB) activity and pro-inflammatory cytokine expression after traumatic brain injury (TBI) in rats.
Right parietal cortical contusion in male rats was made by the weight-dropping method. After trauma, the rats were randomly given chow alone or glutamine mixed chow for 5 d. Gut samples were extracted at 5 d postinjury. We measured NF-kappaB binding activity by electrophoretic mobility shift assay; NF-kappaB subunits p50 and p65 expression by immunohistochemistry; the concentrations of interleukin-1beta, tumor necrosis factor-alpha and interleukin-6 by enzyme-linked immunosorbent assay; intestinal mucosal morphological changes by histopathological study and electron microscopy; and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining.
Administration of glutamine following TBI could decrease NF-kappaB binding activity, NF-kappaB p65 protein expression and concentrations of pro-inflammatory cytokines in the gut. TBI-induced damage of gut structure was ameliorated after glutamine supplementation.
The results of the present study suggest that the therapeutic benefit of post-TBI glutamine supplementation might be due to its inhibitory effects on intestinal NF-kappaB activation and pro-inflammatory cytokine expression.
探讨补充谷氨酰胺是否能调节大鼠创伤性脑损伤（TBI）后肠道核因子κB（NF-κB）活性及促炎细胞因子表达。
采用重物落体法造成雄性大鼠右顶叶皮质挫伤。创伤后，将大鼠随机分为单纯给予饲料组或给予谷氨酰胺混合饲料组，持续5天。在损伤后5天提取肠道样本。通过电泳迁移率变动分析测定NF-κB结合活性；通过免疫组织化学测定NF-κB亚基p50和p65表达；通过酶联免疫吸附测定法测定白细胞介素-1β、肿瘤坏死因子-α和白细胞介素-6的浓度；通过组织病理学研究和电子显微镜观察肠道黏膜形态变化；通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记染色检测细胞凋亡。
TBI后给予谷氨酰胺可降低肠道中NF-κB结合活性、NF-κB p65蛋白表达及促炎细胞因子浓度。补充谷氨酰胺后，TBI诱导的肠道结构损伤得到改善。
本研究结果表明，TBI后补充谷氨酰胺的治疗益处可能归因于其对肠道NF-κB激活和促炎细胞因子表达的抑制作用。
