中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2011年
8期
792-796
,共5页
常瑞明%常建星%温立强%傅玉茹%江志鹏%陈双
常瑞明%常建星%溫立彊%傅玉茹%江誌鵬%陳雙
상서명%상건성%온립강%부옥여%강지붕%진쌍
脓毒症%盲肠结扎穿孔%肠黏膜%修复%杯状细胞%肠三叶因子3%转化生长因子β1%天冬氨酸特异性半胱氨酸蛋白酶
膿毒癥%盲腸結扎穿孔%腸黏膜%脩複%杯狀細胞%腸三葉因子3%轉化生長因子β1%天鼕氨痠特異性半胱氨痠蛋白酶
농독증%맹장결찰천공%장점막%수복%배상세포%장삼협인자3%전화생장인자β1%천동안산특이성반광안산단백매
Sepsis%Cecal ligation and puncture%Intestinal mucosa%Restitution%Goblet cells%Intestinal trefoil factor 3%Transforming growth factor β1%Cysteine-containing aspartate-specific proteases
目的 探讨影响脓毒症肠黏膜损害后修复的因素。方法 采用肓肠结扎穿孔(CLP)所致脓毒症模型，分别以CLP后6，24，48 h不同时间段观测肠黏膜损伤程度和修复过程，前者包括形态学观察及细胞凋亡的测定，后者包括肠黏膜修复的杯状细胞变化、黏膜肠三叶因子3(TFF3)、转化生长因子β1(TGF-β1)以及TNF-α、IL-1含量。结果 形态学观察显示肠黏膜呈持续损害状态，6h的损害积分明显小于24h，48 h组(P＜0.05)，后两组之间差异无统计学意义(P＞0.05)；磷酸化caspase-3蛋白在3组均高于sham组4倍以上；黏膜IL-1，TNF-α含量明显高于sham组3～4倍，其中24h及48 h组明显高于6h组。肠黏膜的修复过程不明显，损伤黏膜未见到明显的杯状细胞积聚；TFF3在6h组轻度增高，24h及48 h组表达下降；杯状细胞数量在CLP的3个组明显减少；TGF-β1在6h组增高，其他两组均接近于sham组。结论 严重脓毒症肠黏膜持续的高炎症状态、杯状细胞功能以及黏膜重建能力下降，影响了受损肠屏障的修复。
目的 探討影響膿毒癥腸黏膜損害後脩複的因素。方法 採用肓腸結扎穿孔(CLP)所緻膿毒癥模型，分彆以CLP後6，24，48 h不同時間段觀測腸黏膜損傷程度和脩複過程，前者包括形態學觀察及細胞凋亡的測定，後者包括腸黏膜脩複的杯狀細胞變化、黏膜腸三葉因子3(TFF3)、轉化生長因子β1(TGF-β1)以及TNF-α、IL-1含量。結果 形態學觀察顯示腸黏膜呈持續損害狀態，6h的損害積分明顯小于24h，48 h組(P＜0.05)，後兩組之間差異無統計學意義(P＞0.05)；燐痠化caspase-3蛋白在3組均高于sham組4倍以上；黏膜IL-1，TNF-α含量明顯高于sham組3～4倍，其中24h及48 h組明顯高于6h組。腸黏膜的脩複過程不明顯，損傷黏膜未見到明顯的杯狀細胞積聚；TFF3在6h組輕度增高，24h及48 h組錶達下降；杯狀細胞數量在CLP的3箇組明顯減少；TGF-β1在6h組增高，其他兩組均接近于sham組。結論 嚴重膿毒癥腸黏膜持續的高炎癥狀態、杯狀細胞功能以及黏膜重建能力下降，影響瞭受損腸屏障的脩複。
목적 탐토영향농독증장점막손해후수복적인소。방법 채용황장결찰천공(CLP)소치농독증모형，분별이CLP후6，24，48 h불동시간단관측장점막손상정도화수복과정，전자포괄형태학관찰급세포조망적측정，후자포괄장점막수복적배상세포변화、점막장삼협인자3(TFF3)、전화생장인자β1(TGF-β1)이급TNF-α、IL-1함량。결과 형태학관찰현시장점막정지속손해상태，6h적손해적분명현소우24h，48 h조(P＜0.05)，후량조지간차이무통계학의의(P＞0.05)；린산화caspase-3단백재3조균고우sham조4배이상；점막IL-1，TNF-α함량명현고우sham조3～4배，기중24h급48 h조명현고우6h조。장점막적수복과정불명현，손상점막미견도명현적배상세포적취；TFF3재6h조경도증고，24h급48 h조표체하강；배상세포수량재CLP적3개조명현감소；TGF-β1재6h조증고，기타량조균접근우sham조。결론 엄중농독증장점막지속적고염증상태、배상세포공능이급점막중건능력하강，영향료수손장병장적수복。
Objective To investigate the unfavorable factors of intestinal mucosa repair after the intestinal epithelial injury in vivo in a mouse model of sepsis. Methods The method of cecal ligature and puncture (CLP) was used to induce sepsis and then the intestinal mucosa damage, epithelial cell apoptosis and the number of transformed goblet cells were observed, and the concentrations of serum TNF-αt, IL-1 and TGF-β1 and TFF3 ( trefoil factor 3) in small intestinal mucosa were determined. All above various laboratory examinations were made by different assays including H-E staining, western blot, ELISA and immunohistochemistry respectively. The experimental mice were divided into sepsis group and sham operation control group. The mice with sepsis were separately sacrificed 6 hours ( n = 7 ), 24 hours ( n = 7) and 48 hours ( n = 7) after CLP. Results In septic mice group, the injured intestinal mucosa was found 6 hours after CLP. The damage scores in mice 24 h and 48 h after CLP were higher than those 6 h after CLP, but there was no significant difference between those 24 h and 48 h after CLP. Moreover, a few goblet cells or other epithelial cells adjacent to the injured surface migrated onto the wound to cover the denuded area. The number of goblet cells was substantially decreased in mice of sepsis group 6 hours after CLP compared with sham operation control group. Compared with sham operation control group, levels of IL-1 and TNF-α significantly increased 3-4 times in mice of sepsis group at all intervals, and the phosphorylated caspase-3 increased 4 times. Although TFF3 assayed by using Western blot showed modest increase 6 h after CLP and it declined 24 h and 48 h later. A similar change was found in TGF-β1, it modestly increased 6h after CLP, but it didn't elevate 24 h and 48 h later. Conclusions Severe sepsis keeps on the inflammatory reaction and epithelial cell apoptosis, preventing the repair of intestinal mucosa from injury.
