中华消化内镜杂志
中華消化內鏡雜誌
중화소화내경잡지
CHINESE JOURNAL OF DIGESTIVE ENDOSCOPY
2009年
1期
35-38
,共4页
陆宗海%林琳%陈蕾%李慧%施瑞华%李学良
陸宗海%林琳%陳蕾%李慧%施瑞華%李學良
륙종해%림림%진뢰%리혜%시서화%리학량
结肠炎,溃疡性%高迁移率族蛋白-1%小鼠%硫酸葡聚糖钠
結腸炎,潰瘍性%高遷移率族蛋白-1%小鼠%硫痠葡聚糖鈉
결장염,궤양성%고천이솔족단백-1%소서%류산포취당납
Colitis,ulcerative%High mobility group box chromosomal protein 1%Mice%Sodium dextran suifate
目的 探讨高迁移率族蛋白-1(HMGB1)在溃疡性结肠炎(UC)发病机制中的作用.方法 BALB/c小鼠32只,随机分成2组,即UX模型组(n=24)和正常对照组(n=8).以3%葡聚糖硫酸钠(DSS)制备小鼠UC模型,造模第24 h、96 h、168 h,分别处死造模组(各8只);对照组正常饮水.观察其病理变化;ELISA法检测血清HMGBl水平;Western-blot法检测结肠组织HMGB1蛋白的表达.结果 随着造模时间的延长,UC组织学评分上升,造模168 h时其结肠黏膜表现与人类UC相类似.UC组血清HMGB1水平在造模24 h时比正常组略升高[(4.49±0.53)μg/L比(5.09±0.61)μg/L,P＞0.05],在96 h达高峰[(14.74±0.60)μg/L,P＜0.01],168 h时峰值下降[(9.03±0.78)μg/L,P＜0.01].UC组小鼠结肠组织HMGB1蛋白表达水平在造模24 h时较正常略升高(0.49±0.03比0.56±0.02,P＞0.05),在造模96 h明显升高(0.76±0.03,P＜0.05),至168 h时仍维持在较高水平(0.77±0.04,P＜0.05).结论 HMGB1在UC小鼠血清中水平升高,结肠组织中也表达明显增强,提示HMGB1作为晚期炎症因子可能参与UC的疾病过程.
目的 探討高遷移率族蛋白-1(HMGB1)在潰瘍性結腸炎(UC)髮病機製中的作用.方法 BALB/c小鼠32隻,隨機分成2組,即UX模型組(n=24)和正常對照組(n=8).以3%葡聚糖硫痠鈉(DSS)製備小鼠UC模型,造模第24 h、96 h、168 h,分彆處死造模組(各8隻);對照組正常飲水.觀察其病理變化;ELISA法檢測血清HMGBl水平;Western-blot法檢測結腸組織HMGB1蛋白的錶達.結果 隨著造模時間的延長,UC組織學評分上升,造模168 h時其結腸黏膜錶現與人類UC相類似.UC組血清HMGB1水平在造模24 h時比正常組略升高[(4.49±0.53)μg/L比(5.09±0.61)μg/L,P＞0.05],在96 h達高峰[(14.74±0.60)μg/L,P＜0.01],168 h時峰值下降[(9.03±0.78)μg/L,P＜0.01].UC組小鼠結腸組織HMGB1蛋白錶達水平在造模24 h時較正常略升高(0.49±0.03比0.56±0.02,P＞0.05),在造模96 h明顯升高(0.76±0.03,P＜0.05),至168 h時仍維持在較高水平(0.77±0.04,P＜0.05).結論 HMGB1在UC小鼠血清中水平升高,結腸組織中也錶達明顯增彊,提示HMGB1作為晚期炎癥因子可能參與UC的疾病過程.
목적 탐토고천이솔족단백-1(HMGB1)재궤양성결장염(UC)발병궤제중적작용.방법 BALB/c소서32지,수궤분성2조,즉UX모형조(n=24)화정상대조조(n=8).이3%포취당류산납(DSS)제비소서UC모형,조모제24 h、96 h、168 h,분별처사조모조(각8지);대조조정상음수.관찰기병리변화;ELISA법검측혈청HMGBl수평;Western-blot법검측결장조직HMGB1단백적표체.결과 수착조모시간적연장,UC조직학평분상승,조모168 h시기결장점막표현여인류UC상유사.UC조혈청HMGB1수평재조모24 h시비정상조략승고[(4.49±0.53)μg/L비(5.09±0.61)μg/L,P＞0.05],재96 h체고봉[(14.74±0.60)μg/L,P＜0.01],168 h시봉치하강[(9.03±0.78)μg/L,P＜0.01].UC조소서결장조직HMGB1단백표체수평재조모24 h시교정상략승고(0.49±0.03비0.56±0.02,P＞0.05),재조모96 h명현승고(0.76±0.03,P＜0.05),지168 h시잉유지재교고수평(0.77±0.04,P＜0.05).결론 HMGB1재UC소서혈청중수평승고,결장조직중야표체명현증강,제시HMGB1작위만기염증인자가능삼여UC적질병과정.
Objective To establish ulcerative colitis(UC)model in BALB/c mice and to investigate the role of high mobility group box chromosomal protein 1(HMGBI)in pathogenesis of UC.Methods Thirty-two BALB/c mice were randomly divided into UC group(n=24,which were fed with 3%dextran sulfate 80dium solution)and control group(n=8,which were fed with water).The animals were sacrificed at 24.96 and 1 68 hours,respectively,to collect samples of colon and blood.The sernm level of HMGB1 was measured with ELISA and the expression of HMGB1 in colon was determined by Western blotting analysis.Results Histological scoring increased with the induction of the model,and manifestation of colon mucosa at 168h was similar with that of UC in human.The serum level of HMGB1 was slightly higer at 24 h than that of control(5.09±0.61 μg/L vs 4.49±0.53μg/L,P＞0.05),and reached a peak at 96 h (14.74±0.60 μg/L,P＜0.01),decreased at 168 h(9.03±0.78μg/L,P＜0.01).The expression 0.05).significandy increased at 96h(0.76±0.03,P＜0.05)and at 168 h(0.77±0.04,P＜0.05).Conclusion HMGB1 might be involved in pathologic changes of UC at a later stage.
