中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2012年
10期
688-692
,共5页
5-氨基水杨酸%结肠炎,溃疡性%结肠肿瘤%疾病模型,动物%PPAR gamma%β-catenin
5-氨基水楊痠%結腸炎,潰瘍性%結腸腫瘤%疾病模型,動物%PPAR gamma%β-catenin
5-안기수양산%결장염,궤양성%결장종류%질병모형,동물%PPAR gamma%β-catenin
Mesalamine%Colitis,ulcerative%Colonic neoplasms%Disease models,animal%PPAR gamma%β-catenin
目的 应用5-氨基水杨酸(5-ASA) 干预偶氮氧甲烷(AOM)联合葡聚糖硫酸钠(DSS)诱导小鼠结肠炎癌变的模型,观察结肠过氧化物酶体增殖物激活受体γ(PPAR-γ)、β-catenin的表达水平.方法 36只BALB/c小鼠均分为对照组、模型组和干预组.模型组和干预组均于实验前1d予AOM 10 mg/kg腹腔注射,继以自由饮用4％DSS 1周,再普通饮水2周,饮用DSS及普通饮水共重复3个循环.干预组于实验前3d予5-ASA 150 mg/kg饲喂至实验结束.对照组于实验前1d予0.9％ NaCl溶液腹腔注射,普通饮水9周.监测小鼠疾病症状,评价实验1周末及9周末结肠组织学病理变化,检测9周末结肠PPAR-γ、β-catenin蛋白及结肠PPAR-γ mRNA表达水平.统计学处理采用t检验.结果 干预组饮用DSS 1周后结肠炎疾病活动指数(DAD为1.81+0.59,9周末平均肿瘤数为4.11±1.05,均较模型组(DAI为2.47±0.53,肿瘤数为9.71±2.29)明显降低(t=2.88和6.55,P均＜0.01).干预组结肠PPAR-γ蛋白(2.11±1.36)及mRNA(1.45±0.10)平均表达水平均较模型组(分别为0.43±0.53,0.57±0.08)明显增加(t=3.07和18.99,P均＜0.01).各组间β-catenin表达差异无统计学意义(P＞0.05).结论 5-ASA有效减轻AOM和DSS诱导的小鼠结肠炎癌变模型的炎性反应及肿瘤负荷,同时促进PPAR-γ在结肠中的表达,而对结肠中β-catenin的表达无明显影响.
目的 應用5-氨基水楊痠(5-ASA) 榦預偶氮氧甲烷(AOM)聯閤葡聚糖硫痠鈉(DSS)誘導小鼠結腸炎癌變的模型,觀察結腸過氧化物酶體增殖物激活受體γ(PPAR-γ)、β-catenin的錶達水平.方法 36隻BALB/c小鼠均分為對照組、模型組和榦預組.模型組和榦預組均于實驗前1d予AOM 10 mg/kg腹腔註射,繼以自由飲用4％DSS 1週,再普通飲水2週,飲用DSS及普通飲水共重複3箇循環.榦預組于實驗前3d予5-ASA 150 mg/kg飼餵至實驗結束.對照組于實驗前1d予0.9％ NaCl溶液腹腔註射,普通飲水9週.鑑測小鼠疾病癥狀,評價實驗1週末及9週末結腸組織學病理變化,檢測9週末結腸PPAR-γ、β-catenin蛋白及結腸PPAR-γ mRNA錶達水平.統計學處理採用t檢驗.結果 榦預組飲用DSS 1週後結腸炎疾病活動指數(DAD為1.81+0.59,9週末平均腫瘤數為4.11±1.05,均較模型組(DAI為2.47±0.53,腫瘤數為9.71±2.29)明顯降低(t=2.88和6.55,P均＜0.01).榦預組結腸PPAR-γ蛋白(2.11±1.36)及mRNA(1.45±0.10)平均錶達水平均較模型組(分彆為0.43±0.53,0.57±0.08)明顯增加(t=3.07和18.99,P均＜0.01).各組間β-catenin錶達差異無統計學意義(P＞0.05).結論 5-ASA有效減輕AOM和DSS誘導的小鼠結腸炎癌變模型的炎性反應及腫瘤負荷,同時促進PPAR-γ在結腸中的錶達,而對結腸中β-catenin的錶達無明顯影響.
목적 응용5-안기수양산(5-ASA) 간예우담양갑완(AOM)연합포취당류산납(DSS)유도소서결장염암변적모형,관찰결장과양화물매체증식물격활수체γ(PPAR-γ)、β-catenin적표체수평.방법 36지BALB/c소서균분위대조조、모형조화간예조.모형조화간예조균우실험전1d여AOM 10 mg/kg복강주사,계이자유음용4％DSS 1주,재보통음수2주,음용DSS급보통음수공중복3개순배.간예조우실험전3d여5-ASA 150 mg/kg사위지실험결속.대조조우실험전1d여0.9％ NaCl용액복강주사,보통음수9주.감측소서질병증상,평개실험1주말급9주말결장조직학병리변화,검측9주말결장PPAR-γ、β-catenin단백급결장PPAR-γ mRNA표체수평.통계학처리채용t검험.결과 간예조음용DSS 1주후결장염질병활동지수(DAD위1.81+0.59,9주말평균종류수위4.11±1.05,균교모형조(DAI위2.47±0.53,종류수위9.71±2.29)명현강저(t=2.88화6.55,P균＜0.01).간예조결장PPAR-γ단백(2.11±1.36)급mRNA(1.45±0.10)평균표체수평균교모형조(분별위0.43±0.53,0.57±0.08)명현증가(t=3.07화18.99,P균＜0.01).각조간β-catenin표체차이무통계학의의(P＞0.05).결론 5-ASA유효감경AOM화DSS유도적소서결장염암변모형적염성반응급종류부하,동시촉진PPAR-γ재결장중적표체,이대결장중β-catenin적표체무명현영향.
Objective To investigate the expressions of peroxisome proliferator activated receptor-γ (PPAR-γ) and β-catenin in 5-aminosalicylic acid （ASA) intervened colitis carcinogenesis mouse model induced by azoxymethane (AOM) and dextran sulfate sodium (DSS).Methods Thirtysix BALB/c mice were evenly divided into control group,model group,and intervention group.For model group and intervention group,mice were intraperitoneally injected with AOM (10 mg/kg) one day before experiment,then drank 4％ DSS solution freely for one week and followed with common drinking water for another two weeks.Taking 4％ DSS solution and common drinking water repeated for three cycles.For intervention group,5-ASA (150 mg/kg) was given from three days before experiment to the end of research.For control group,mice were intraperitoneally injected with 0.9％NaCl solation and then given common drinking water for nine weeks.The symptoms of the disease were monitored in mice and pathological changes of tissues were evaluated at the end of first week and ninth week.At the end of the ninth week,the expressions of PPAR-γ,β-catenin protein and PPAR-γat mRNA level in colon tissue were detected.The data were analyzed by t test.Results The colitis disease activity index (DAI) index of intervention group was 1.81 ±0.59 after drinking DSS solution for one week and the number of tumor was 4.11 ± 1.05 at the end of the ninth week,both were significantly lower than those of model group (2.47 ± 0.53 and 9.71±2.29 respectively,t=2.88 and 6.55; both P＜0.01).The expression of PPAR-γ at protein level (2.11±1.36) and mRNA level (1.45±0.10) in colon tissue of intervention group significantly increased compared with those of model group (0.43±0.53 and 0.57±0.08 respectively,t=3.07 and 18.99,both P＜0.01).There was no significant difference of β-catenin expression among groups (P＞0.05).Conclusions 5-ASA can efficiently improve the inflammatory reaction and tumor load in AOM and DSS induced colitis carcinogenesis mouse model,and at the same time can promote the expression of PPAR-γ in colon.However,there was no significant influence on the expression of β-catenin.
