世界中西医结合杂志
世界中西醫結閤雜誌
세계중서의결합잡지
WORLD JOURNAL OF TRADITIONAL CHINESE AND WESTERN MEDICINE
2014年
5期
473-476,491
,共5页
吴昊%沈洪%朱磊%朱萱萱%刘军楼%欧阳俊%谷静
吳昊%瀋洪%硃磊%硃萱萱%劉軍樓%歐暘俊%穀靜
오호%침홍%주뢰%주훤훤%류군루%구양준%곡정
清肠化湿方%Caspase-3%ZO-1%溃疡性结肠炎%核因子-κB
清腸化濕方%Caspase-3%ZO-1%潰瘍性結腸炎%覈因子-κB
청장화습방%Caspase-3%ZO-1%궤양성결장염%핵인자-κB
QIngchang Huashi Formula%Caspase-3%ZO1%Ulcerative Colitis%NF-κB
目的：以核因子-κB（ nuclear facter-κB，NF-κB）p65反义寡核苷酸（ ASODN）及西药柳氮磺胺吡啶（ SASP）为对照，观察清肠化湿方对三硝基苯磺酸（ TNBS）法诱导小鼠溃疡性结肠炎（UC）模型结肠黏膜天冬氨酸特异酶切的半胱氨酸蛋白酶-3（Caspase-3）、闭锁小带蛋白-1（ZO-1）表达的影响。方法采用TNBS诱导小鼠UC模型，并随机分为清肠化湿方组、SASP组、清肠化湿方=SASP组、ASODN组、模型对照组、空白对照组，治疗7 d后处死小鼠，取小鼠结肠标本，采用HE染色法观察各组小鼠结肠病理形态，并采用Western blot法检测各组小鼠结肠上皮细胞Caspase-3及ZO-1蛋白表达水平。结果模型对照组小鼠 Caspase -3蛋白表达明显高于空白对照组（ P ﹤0.05）；清肠化湿方组Caspase-3蛋白表达低于模型对照组（ P﹤0.05），与空白对照组比较差异无统计学意义（P﹥0.05）。模型对照组小鼠ZO-1蛋白表达明显低于空白对照组（P﹤0.05）；清肠化湿方组ZO-1蛋白表达高于模型对照组（P﹤0.05），与空白对照组比较差异无统计学意义（P﹥0.05）。结论清肠化湿方对UC模型小鼠具有治疗作用，其抑制肠上皮细胞Caspase-3蛋白表达、增强ZO-1的表达，抑制肠黏膜组织细胞凋亡，恢复正常的肠黏膜屏障形态和功能可能是其作用机制的一部分。
目的：以覈因子-κB（ nuclear facter-κB，NF-κB）p65反義寡覈苷痠（ ASODN）及西藥柳氮磺胺吡啶（ SASP）為對照，觀察清腸化濕方對三硝基苯磺痠（ TNBS）法誘導小鼠潰瘍性結腸炎（UC）模型結腸黏膜天鼕氨痠特異酶切的半胱氨痠蛋白酶-3（Caspase-3）、閉鎖小帶蛋白-1（ZO-1）錶達的影響。方法採用TNBS誘導小鼠UC模型，併隨機分為清腸化濕方組、SASP組、清腸化濕方=SASP組、ASODN組、模型對照組、空白對照組，治療7 d後處死小鼠，取小鼠結腸標本，採用HE染色法觀察各組小鼠結腸病理形態，併採用Western blot法檢測各組小鼠結腸上皮細胞Caspase-3及ZO-1蛋白錶達水平。結果模型對照組小鼠 Caspase -3蛋白錶達明顯高于空白對照組（ P ﹤0.05）；清腸化濕方組Caspase-3蛋白錶達低于模型對照組（ P﹤0.05），與空白對照組比較差異無統計學意義（P﹥0.05）。模型對照組小鼠ZO-1蛋白錶達明顯低于空白對照組（P﹤0.05）；清腸化濕方組ZO-1蛋白錶達高于模型對照組（P﹤0.05），與空白對照組比較差異無統計學意義（P﹥0.05）。結論清腸化濕方對UC模型小鼠具有治療作用，其抑製腸上皮細胞Caspase-3蛋白錶達、增彊ZO-1的錶達，抑製腸黏膜組織細胞凋亡，恢複正常的腸黏膜屏障形態和功能可能是其作用機製的一部分。
목적：이핵인자-κB（ nuclear facter-κB，NF-κB）p65반의과핵감산（ ASODN）급서약류담광알필정（ SASP）위대조，관찰청장화습방대삼초기분광산（ TNBS）법유도소서궤양성결장염（UC）모형결장점막천동안산특이매절적반광안산단백매-3（Caspase-3）、폐쇄소대단백-1（ZO-1）표체적영향。방법채용TNBS유도소서UC모형，병수궤분위청장화습방조、SASP조、청장화습방=SASP조、ASODN조、모형대조조、공백대조조，치료7 d후처사소서，취소서결장표본，채용HE염색법관찰각조소서결장병리형태，병채용Western blot법검측각조소서결장상피세포Caspase-3급ZO-1단백표체수평。결과모형대조조소서 Caspase -3단백표체명현고우공백대조조（ P ﹤0.05）；청장화습방조Caspase-3단백표체저우모형대조조（ P﹤0.05），여공백대조조비교차이무통계학의의（P﹥0.05）。모형대조조소서ZO-1단백표체명현저우공백대조조（P﹤0.05）；청장화습방조ZO-1단백표체고우모형대조조（P﹤0.05），여공백대조조비교차이무통계학의의（P﹥0.05）。결론청장화습방대UC모형소서구유치료작용，기억제장상피세포Caspase-3단백표체、증강ZO-1적표체，억제장점막조직세포조망，회복정상적장점막병장형태화공능가능시기작용궤제적일부분。
Objective To take NF-κB p65 ASODN and the western medicine SASP as the controls to observe the impacts of Qingchang Huashi Formula on the expressions of Caspase-3 and ZO-1 in ulcera-tive colitis( UC)models of mice induced by TNBS methods. Methods TNBS method was adopted to induce UC models,which were randomized into a Qingchang Huashi Formula group( Formula group),a SASP group, Formula = SASP group,ASODN group,a model control group and a blank control group. The mice were sac-rificed in 7 days of treatment and the colon samples were collected. HE method was used to observe the path-ologic morphology of colons in the experimental mice in each group. Western Blot method was applied to de-termine the expressions of Caspase-3 and ZO-1 in each group. Results Capspase-3 expression in the model control group was higher apparently than that in the blank control group(P﹤0. 05),Capsase-3 ex-pression in the Formula group was lower than that in the model control group(P﹤0. 05),but had no statisti-cal difference as compared with the blank control group(P﹥0. 05). ZO-1 expression in the model control group was lower apparently than that in the blank control group(P﹤0. 05),that in the Formula group was higher than that in the model control group(P﹤0. 05),but had no statistical difference as compared with the blank control group(P﹥0. 05). Conclusion Qingchang Huashi Formula had the therapeutic effect on UC models of mice. It suppresses epithelial cell Caspase-3 expression and intensifies ZO-1 expression,inhibits intestinal mucosal apoptosis and recovers the normal morphology and function of intestinal mucosal barrier. All of those could be the effect mechanism of the formula.
