中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2010年
1期
33-37,插2
,共6页
卢春玉%汪健%黄顺根%李萍%金美芳
盧春玉%汪健%黃順根%李萍%金美芳
로춘옥%왕건%황순근%리평%금미방
肠外营养%基因芯片%炎症细胞因子%受体
腸外營養%基因芯片%炎癥細胞因子%受體
장외영양%기인심편%염증세포인자%수체
Parenteral nutrition%Gene chip%Inflammatory cytokines%Receptors
目的 研究肠外营养(PN)对大鼠肠道炎症因子及其受体基因表达的影响,探讨其在PN相关肠道损害中的作用.方法 12只雄性Sprague-Dawley远交群大鼠分为PN组和对照组,每组6只.每只大鼠均经颈静脉置入硅胶管.PN组大鼠在禁食、禁水的同时,经颈静脉硅胶管连续24 h输注营养液,对照组采用普通饮食喂养的同时经颈静脉硅胶管输注生理盐水.7 d后取空肠组织分别采用电子显微镜和实时定量PCR芯片检测大鼠空肠的超微结构和肠道炎症因子及其受体基因的表达情况.结果 电子显微镜显示,PN组大鼠空肠肠壁微绒毛横断面微绒毛变短萎缩,线粒体肿胀,黏膜下层可见较多凋亡小体,细胞间连接紊乱断裂;而对照组大鼠空肠超微结构正常.PN组白细胞介素1受体1、白细胞介素8受体b、γ干扰素基因的表达较对照组上调,CC型趋化因子配体17(CCL17)、CCL19、CCL21、CXC型趋化因子受体3(CXCR3)、CCL22、CCL9、CC型趋化因子受体3(CCR3)、CCR7、CCR5、C反应蛋白、白细胞介素10基因的表达较对照组下调.结论 PN对大鼠肠道炎症因子及受体基因的表达有影响,其中细胞因子γ干扰素表达上调,白细胞介素10表达下调,趋化因子及受体CCL19、CCL21、CCR3、CXCR3、CCR7和CCR5表达下调可能与PN引起的肠道机械和免疫功能损伤有关.
目的 研究腸外營養(PN)對大鼠腸道炎癥因子及其受體基因錶達的影響,探討其在PN相關腸道損害中的作用.方法 12隻雄性Sprague-Dawley遠交群大鼠分為PN組和對照組,每組6隻.每隻大鼠均經頸靜脈置入硅膠管.PN組大鼠在禁食、禁水的同時,經頸靜脈硅膠管連續24 h輸註營養液,對照組採用普通飲食餵養的同時經頸靜脈硅膠管輸註生理鹽水.7 d後取空腸組織分彆採用電子顯微鏡和實時定量PCR芯片檢測大鼠空腸的超微結構和腸道炎癥因子及其受體基因的錶達情況.結果 電子顯微鏡顯示,PN組大鼠空腸腸壁微絨毛橫斷麵微絨毛變短萎縮,線粒體腫脹,黏膜下層可見較多凋亡小體,細胞間連接紊亂斷裂;而對照組大鼠空腸超微結構正常.PN組白細胞介素1受體1、白細胞介素8受體b、γ榦擾素基因的錶達較對照組上調,CC型趨化因子配體17(CCL17)、CCL19、CCL21、CXC型趨化因子受體3(CXCR3)、CCL22、CCL9、CC型趨化因子受體3(CCR3)、CCR7、CCR5、C反應蛋白、白細胞介素10基因的錶達較對照組下調.結論 PN對大鼠腸道炎癥因子及受體基因的錶達有影響,其中細胞因子γ榦擾素錶達上調,白細胞介素10錶達下調,趨化因子及受體CCL19、CCL21、CCR3、CXCR3、CCR7和CCR5錶達下調可能與PN引起的腸道機械和免疫功能損傷有關.
목적 연구장외영양(PN)대대서장도염증인자급기수체기인표체적영향,탐토기재PN상관장도손해중적작용.방법 12지웅성Sprague-Dawley원교군대서분위PN조화대조조,매조6지.매지대서균경경정맥치입규효관.PN조대서재금식、금수적동시,경경정맥규효관련속24 h수주영양액,대조조채용보통음식위양적동시경경정맥규효관수주생리염수.7 d후취공장조직분별채용전자현미경화실시정량PCR심편검측대서공장적초미결구화장도염증인자급기수체기인적표체정황.결과 전자현미경현시,PN조대서공장장벽미융모횡단면미융모변단위축,선립체종창,점막하층가견교다조망소체,세포간련접문란단렬;이대조조대서공장초미결구정상.PN조백세포개소1수체1、백세포개소8수체b、γ간우소기인적표체교대조조상조,CC형추화인자배체17(CCL17)、CCL19、CCL21、CXC형추화인자수체3(CXCR3)、CCL22、CCL9、CC형추화인자수체3(CCR3)、CCR7、CCR5、C반응단백、백세포개소10기인적표체교대조조하조.결론 PN대대서장도염증인자급수체기인적표체유영향,기중세포인자γ간우소표체상조,백세포개소10표체하조,추화인자급수체CCL19、CCL21、CCR3、CXCR3、CCR7화CCR5표체하조가능여PN인기적장도궤계화면역공능손상유관.
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.
