海南医学
海南醫學
해남의학
Hainan Medical Journal
2015年
21期
3124-3126
,共3页
同种异体移植物炎症因子-1%白细胞介素-1β%溃疡性结肠炎%致病机制
同種異體移植物炎癥因子-1%白細胞介素-1β%潰瘍性結腸炎%緻病機製
동충이체이식물염증인자-1%백세포개소-1β%궤양성결장염%치병궤제
Allograft inflammatory factor-1 (AIF-1)%Interleukin-1β(IL-1β)%Ulcerative colitis%Pathogenesis
目的 探讨同种异体移植物炎症因子-1 (AIF-1)及白细胞介素-1β(IL-1β)在溃疡性结肠炎致病机制中的作用.方法 90只BALB/c小鼠随机分为三组,每组30只,第1组用葡聚糖硫酸钠(DSS)造模为溃疡性结肠炎,第2组用大肠杆菌造模为细菌性肠炎,第3组为正常对照,取得各组小鼠的外周血及结肠标本,用ELISA的方法检测AIF-1、IL-1β的表达,比较其在三组小鼠体内表达的差异.结果 (1)溃疡性结肠炎小鼠AIF-1表达水平分别为外周血中(0.134±0.048) ng/ml,结肠中(0.462±0.117) ng/ml,均较细菌性肠炎[外周血中(1.425±0.229) ng/ml、结肠中(1.261±0.48)] ng/ml高,各组间比较差异均有统计学意义(P<0.05);(2)溃疡性结肠炎小鼠IL-1β表达分别为外周血中(0.894 ± 0.173) ng/ml,结肠中(1.261 ± 0.048) ng/ml,与细菌性肠炎[外周血中(0.087 ± 0.021) ng/ml、结肠中(0.149±0.057) ng/ml]比较差异均无统计学意义(P>0.05);(3)溃疡性结肠炎及细菌性肠炎小鼠AIF-1与IL-1β表达水平无相关性(P>0.05).结论 AIF-1可能参与了溃疡性结肠炎的特异性致病机制,IL-1β可能未参与特异性致病机制.
目的 探討同種異體移植物炎癥因子-1 (AIF-1)及白細胞介素-1β(IL-1β)在潰瘍性結腸炎緻病機製中的作用.方法 90隻BALB/c小鼠隨機分為三組,每組30隻,第1組用葡聚糖硫痠鈉(DSS)造模為潰瘍性結腸炎,第2組用大腸桿菌造模為細菌性腸炎,第3組為正常對照,取得各組小鼠的外週血及結腸標本,用ELISA的方法檢測AIF-1、IL-1β的錶達,比較其在三組小鼠體內錶達的差異.結果 (1)潰瘍性結腸炎小鼠AIF-1錶達水平分彆為外週血中(0.134±0.048) ng/ml,結腸中(0.462±0.117) ng/ml,均較細菌性腸炎[外週血中(1.425±0.229) ng/ml、結腸中(1.261±0.48)] ng/ml高,各組間比較差異均有統計學意義(P<0.05);(2)潰瘍性結腸炎小鼠IL-1β錶達分彆為外週血中(0.894 ± 0.173) ng/ml,結腸中(1.261 ± 0.048) ng/ml,與細菌性腸炎[外週血中(0.087 ± 0.021) ng/ml、結腸中(0.149±0.057) ng/ml]比較差異均無統計學意義(P>0.05);(3)潰瘍性結腸炎及細菌性腸炎小鼠AIF-1與IL-1β錶達水平無相關性(P>0.05).結論 AIF-1可能參與瞭潰瘍性結腸炎的特異性緻病機製,IL-1β可能未參與特異性緻病機製.
목적 탐토동충이체이식물염증인자-1 (AIF-1)급백세포개소-1β(IL-1β)재궤양성결장염치병궤제중적작용.방법 90지BALB/c소서수궤분위삼조,매조30지,제1조용포취당류산납(DSS)조모위궤양성결장염,제2조용대장간균조모위세균성장염,제3조위정상대조,취득각조소서적외주혈급결장표본,용ELISA적방법검측AIF-1、IL-1β적표체,비교기재삼조소서체내표체적차이.결과 (1)궤양성결장염소서AIF-1표체수평분별위외주혈중(0.134±0.048) ng/ml,결장중(0.462±0.117) ng/ml,균교세균성장염[외주혈중(1.425±0.229) ng/ml、결장중(1.261±0.48)] ng/ml고,각조간비교차이균유통계학의의(P<0.05);(2)궤양성결장염소서IL-1β표체분별위외주혈중(0.894 ± 0.173) ng/ml,결장중(1.261 ± 0.048) ng/ml,여세균성장염[외주혈중(0.087 ± 0.021) ng/ml、결장중(0.149±0.057) ng/ml]비교차이균무통계학의의(P>0.05);(3)궤양성결장염급세균성장염소서AIF-1여IL-1β표체수평무상관성(P>0.05).결론 AIF-1가능삼여료궤양성결장염적특이성치병궤제,IL-1β가능미삼여특이성치병궤제.
Objective To explore the roles of allograft inflammatory factor-1 (AIF-1) and interleukin-1β(IL-1β) in the pathogenesis of ulcerative colitis. Methods Ninety BALB/c mice were randomly divided into three groups, each with 30 mices. In group 1, dextran sulphate sodium (DSS) was applied for modeling of ulcerative colitis, and E. coli was applied for modeling of bacterial enteritis in Group 2. Group 3 was set as the normal control. Peripheral blood samples and colon tissues of mice were collected for detection of AIF-1 and IL-1βexpression level by ELISA. Results (1) In group 1, AIF-1 expression levels were (0.134±0.048) ng/ml in peripheral blood and (0.462±0.117) ng/ml in colon tissues, which were significantly higher than the levels in group 2 [(1.425 ± 0.229) ng/ml in peripheral blood, (1.261±0.48) ng/ml in colon tissues], P<0.05. (2) There was no statistically significant difference in IL-1βexpression level between group 1 [(0.894 ± 0.173) ng/ml in peripheral blood, (1.261 ± 0.048) ng/ml in colon tissues] and group 2 [(0.087±0.021) in peripheral blood, (0.149±0.057) in colon tissues], P>0.05. (3) AIF-1 and IL-1βexpression levels in mice of bacterial enteritis or ulcerative colitis had no relevance (P>0.05). Conclusion AIF-1 might be involved in the specific pathogenesis of ulcerative colitis, and IL-1βmay not participate in the pathogenesis.
