Effects of parenteral nutrition on the gene expressions of rat intestinal inflammatory cytokines and receptors / 中华临床营养杂志

ABSTRACT

@#Objective To identify the effects of parenteral nutrition (PN) on the gene expressions of rat intestinal inflammatory cytokincs and receptors and to explore the role of these changes in PN-related intestinal impairment. Methods Totally 12 male Sprague-Dawley rats were equally divided into the control group and the PN group. A silastic catheter was inserted into the right jugular vein of each rat. No food or water was administered to the PN group except for a continuous 24-hour PN infusion through the silastic catheter in the jugular vein. The control group, while being regularly fed, was administered with an infusion of normal saline through the silastic catheter in thc jugular vein. After 7 days, intestinal tissues were taken for electron microscopy and real-time PCR array to analyze thc microstructure change in rat intestine and thc gene expressions of inflammatory cytokines and their receptors. Results Electron microscopy revealed atrophy of microvillus, engorgement of mitochondria, cell-cell junction breakage, and several apoptotic bodies in the PN group and normal intestinal microstructure in the control group. Compared with the control group, the PN group showed an up-regulation in the gene expressions of interferon γ, interleukin-1 receptor type I , interlcukin-8 receptor type b and a down-regulation in the gene expressions of CC chemokine ligand 17 (CCL17) , CCL19, CCL21, CCL22, CCL9, CXC chemokine receptor 3, CC chemokine receptor 3 ( CCP3 ), CCR7, CCR5, C-reactive protein, and interleukin-10. Conclusions PN influences the gene expressions of rat intestinal inflammatory cytokincs and receptors. The expression of cytokine interferon γ increases and that of interleukin-10 declines, and the expressions of CCL19, CCL21, CXC chemokine receptor 3, CCR3,CCR7, and CCR5 decline. The alterations of these genes may be associated with the impairment of intestinal immune and mechanical functions.