CAJ | 학술논문

目的观察雷帕霉素对大鼠肝内胆管缺血后磷酸化p70S6激酶含量的影响.方法将120只雄性SD大鼠随机分4组:A组为对照组(假手术组)28只,B组为假手术+雷帕霉素组28只;C组为缺血组32只,D组为缺血+雷帕霉素组32只.雷帕霉素按每天2.0 mg/kg大鼠胃内注入.各实验组于术后第1、3、7天分别处死6只大鼠,术后14 d处死全部大鼠.切取肝脏组织,Western blot 检测磷酸化p70S6激酶(p-p70s6k)含量.多个独立样本比较采用Kruskal-Wallis H检验,两样本间的比较经秩转换处理后行One Way ANOVA检验,两独立样本比较采用Mann-Whitney U检验.结果缺血组p-p70S6k含量增加,术后7d达峰值(4.81 ±0.45),为对照组9.64倍(P＜0.01);雷帕霉素处理后,p-p70S6k含量术后无明显增加,术后3、7d其含量明显低于缺血组(P＜0.01).结论雷帕霉素抑制胆管缺血后p70s6k磷酸化,影响p-p70S6k的生成,这是雷帕霉素抑制胆管缺血后代偿性增生的机制之一.
목적 관찰뢰파매소대대서간내담관결혈후린산화p70S6격매함량적영향.방법 장120지웅성SD대서수궤분4조:A조위대조조(가수술조)28지,B조위가수술+뢰파매소조28지;C조위결혈조32지,D조위결혈+뢰파매소조32지.뢰파매소안매천2.0 mg/kg대서위내주입.각실험조우술후제1、3、7천분별처사6지대서,술후14 d처사전부대서.절취간장조직,Western blot 검측린산화p70S6격매(p-p70s6k)함량.다개독립양본비교채용Kruskal-Wallis H검험,량양본간적비교경질전환처리후행One Way ANOVA검험,량독립양본비교채용Mann-Whitney U검험.결과 결혈조p-p70S6k함량증가,술후7d체봉치(4.81 ±0.45),위대조조9.64배(P＜0.01);뢰파매소처리후,p-p70S6k함량술후무명현증가,술후3、7d기함량명현저우결혈조(P＜0.01).결론 뢰파매소억제담관결혈후p70s6k린산화,영향p-p70S6k적생성,저시뢰파매소억제담관결혈후대상성증생적궤제지일.
Objective To investigate the effect of rapamycin on phosphorylated p70s6 kinase (p-p70s6k) after deprivation of biliary blood supply.Methods Male SD rats were randomly assigned into 4 groups:sham (n =28),sham + rapamycin (n =28),ischemia (n =32) and ischemia + rapamycin (n =32).In ischemia group,complete deprivation of bile duct arterial supply was performed,and in sham group,open-close operation was carried out.Daily intake of rapamycin (2 mg/kg) was given in rapamycin treated groups with the same volume of saline in non-rapamycin treated groups.Six rats were sacrificed on the postoperative day (POD) 1,3 and 7,and the rest sacrificed on the POD 14.Fresh liver tissues were obtained,followed by Western blotting for detection of p-p70S6k content.Kruskal-Wallis H test was used for comparion of multiple independent samples and the following pairwise comparisons were performed by rank transformation and One Way ANOVA.Difference between two independent samples was determined by Mann-Whitney U test.Results Western blotting showed that p-p70S6k was up-regulated in ischemia group,with the peak level (4.81 ±0.45) of 9.64 folds to sham group (P ＜0.01).With administration of rapamycin,there was no increase of p-p70S6k content in biliary ischemic rats.Further more,on the POD 3 and 7,p-p70S6k in ischemia + rapamycin group was lower than that in ischemia group (P ＜ 0.01).Conclusion Rapamycin inhibits phosphorylation of p70S6k,which provides explanation to negative effect of rapamycin on adaptive bile duct proliferation in response to ischemia.