广西医学
廣西醫學
엄서의학
GUANGXI MEDICAL JOURNAL
2014年
10期
1377-1380
,共4页
严彩霞%张丙宏%张海霞%赵日红
嚴綵霞%張丙宏%張海霞%趙日紅
엄채하%장병굉%장해하%조일홍
坏死性小肠结肠炎%肠三叶因子%大鼠%p-BAD蛋白%磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶信号转导
壞死性小腸結腸炎%腸三葉因子%大鼠%p-BAD蛋白%燐脂酰肌醇-3激酶/絲氨痠-囌氨痠蛋白激酶信號轉導
배사성소장결장염%장삼협인자%대서%p-BAD단백%린지선기순-3격매/사안산-소안산단백격매신호전도
Necrotizing enterocolitis%Intestinal trefoil factor%Rat%p-BAD protein%Phosphoinositide-3 kinase /serine/threonine kinase transduction
目的：观察肠三叶因子（ITF）对新生鼠坏死性小肠结肠炎（NEC）模型磷酸化丝氨酸-苏氨酸蛋白激酶（p-AKT）及磷酸化 BAD（p-BAD）蛋白水平的影响，探讨 ITF 对 NEC 的保护作用。方法新生鼠50只，随机分为5组，每组10只。建立 NEC 模型，A 组腹腔注射生理盐水0．2 ml；B 组腹腔注射 ITF 0．2 mg；C 组腹腔内注射渥漫青霉素0．1 mg/kg；D 组腹腔内注射 ITF 0．2 mg ＋渥漫青霉素0．1 mg/kg；E 组为正常对照组。实验第4天断头处死大鼠，取近回盲部肠道组织做病理学检查，分别采用免疫组化方法及免疫印迹法检测肠组织中 p-AKT 及 p-BAD 蛋白表达水平。结果5组肠组织中 p-AKT 及 p-BAD 蛋白表达水平比较，差异有统计学意义（P 均＜0．05），B 组 p-AKT、p-BAD 蛋白表达水平高于其他4组（P 均＜0．05），A 组高于 E 组（P 均＜0．05）， C 组 p-AKT 最低（P ＜0．05）。各组大鼠肠损伤病理评分比较，差异有统计学意义（P ＜0．05），A、C、D 组肠损伤病理评分高于 B 组（P ＜0．05）。结论ITF 可减轻新生鼠 NEC 的肠道炎症反应，其机制可能是使 AKT 活化为p-AKT，其作用于下游靶点 p-BAD，抑制 BAD 的促凋亡作用。
目的：觀察腸三葉因子（ITF）對新生鼠壞死性小腸結腸炎（NEC）模型燐痠化絲氨痠-囌氨痠蛋白激酶（p-AKT）及燐痠化 BAD（p-BAD）蛋白水平的影響，探討 ITF 對 NEC 的保護作用。方法新生鼠50隻，隨機分為5組，每組10隻。建立 NEC 模型，A 組腹腔註射生理鹽水0．2 ml；B 組腹腔註射 ITF 0．2 mg；C 組腹腔內註射渥漫青黴素0．1 mg/kg；D 組腹腔內註射 ITF 0．2 mg ＋渥漫青黴素0．1 mg/kg；E 組為正常對照組。實驗第4天斷頭處死大鼠，取近迴盲部腸道組織做病理學檢查，分彆採用免疫組化方法及免疫印跡法檢測腸組織中 p-AKT 及 p-BAD 蛋白錶達水平。結果5組腸組織中 p-AKT 及 p-BAD 蛋白錶達水平比較，差異有統計學意義（P 均＜0．05），B 組 p-AKT、p-BAD 蛋白錶達水平高于其他4組（P 均＜0．05），A 組高于 E 組（P 均＜0．05）， C 組 p-AKT 最低（P ＜0．05）。各組大鼠腸損傷病理評分比較，差異有統計學意義（P ＜0．05），A、C、D 組腸損傷病理評分高于 B 組（P ＜0．05）。結論ITF 可減輕新生鼠 NEC 的腸道炎癥反應，其機製可能是使 AKT 活化為p-AKT，其作用于下遊靶點 p-BAD，抑製 BAD 的促凋亡作用。
목적：관찰장삼협인자（ITF）대신생서배사성소장결장염（NEC）모형린산화사안산-소안산단백격매（p-AKT）급린산화 BAD（p-BAD）단백수평적영향，탐토 ITF 대 NEC 적보호작용。방법신생서50지，수궤분위5조，매조10지。건립 NEC 모형，A 조복강주사생리염수0．2 ml；B 조복강주사 ITF 0．2 mg；C 조복강내주사악만청매소0．1 mg/kg；D 조복강내주사 ITF 0．2 mg ＋악만청매소0．1 mg/kg；E 조위정상대조조。실험제4천단두처사대서，취근회맹부장도조직주병이학검사，분별채용면역조화방법급면역인적법검측장조직중 p-AKT 급 p-BAD 단백표체수평。결과5조장조직중 p-AKT 급 p-BAD 단백표체수평비교，차이유통계학의의（P 균＜0．05），B 조 p-AKT、p-BAD 단백표체수평고우기타4조（P 균＜0．05），A 조고우 E 조（P 균＜0．05）， C 조 p-AKT 최저（P ＜0．05）。각조대서장손상병리평분비교，차이유통계학의의（P ＜0．05），A、C、D 조장손상병리평분고우 B 조（P ＜0．05）。결론ITF 가감경신생서 NEC 적장도염증반응，기궤제가능시사 AKT 활화위p-AKT，기작용우하유파점 p-BAD，억제 BAD 적촉조망작용。
Objective To observe the effects of intestinal trefoil factor (ITF) on the levels of p-AKT and p-BAD in the necrotizing enterocolitis (NEC) model of neonatal rat ,and to investigate the protective effect of ITF on NEC . Methods Fifty neonatal rats were randomly divided into 5 groups,with 10 rats in each group.The NEC model of neonatal rats was established.Group A was given intraperitoneal injection of normal saline(0.2 ml),group B was given intraperitoneal injection of ITF(0.2 mg),group C was given intraperitoneal injection of wortmannin (0.1 mg/kg),group D was given intraperitoneal injection of ITF(0.2 mg) and wortmannin(0.1 mg/kg),and group E as normal control group .All the subjects were put to death on the 4th day after experiment.The intestinal tissues located at the boundary of ileum and cecum were obtained to observe histological changes .Immunohistochemical method and Western Blot were used to detect the levels of p-AKT and p-BAD in intestinal tissues.Results There were significant differences in the levels of p -AKT and p-BAD in intestinal tissues among 5 groups(P <0.05).The levels of p-AKT and p-BAD in group B were higher than those in other four groups (all P <0.05).The levels of p-AKT and p-BAD in group A were higher than those in group E(all P <0.05).The level of p-AKT was the weakest in group C (P <0.05).There was significant difference in the pathology score of intestinal injury among groups (P <0.05).The pathology score of intestinal injury in group A , group C and group D was higher than that in group B(P <0.05).Conclusion ITF might relieve the intestinal inflammation of neonatal rats with NEC by AKT activation to p-AKT.It might play a role in p-BAD,and suppress the apoptosis-promoting effect of BAD.
