中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2013年
4期
259-263
,共5页
郭东梅%周超%白研%白文元
郭東梅%週超%白研%白文元
곽동매%주초%백연%백문원
Barrett食管%受体,表皮生长因子%1-磷脂酰肌醇3激酶%蛋白质丝氨酸苏氨酸激酶%信号转导%疾病模型,动物
Barrett食管%受體,錶皮生長因子%1-燐脂酰肌醇3激酶%蛋白質絲氨痠囌氨痠激酶%信號轉導%疾病模型,動物
Barrett식관%수체,표피생장인자%1-린지선기순3격매%단백질사안산소안산격매%신호전도%질병모형,동물
Barrett esophagus%Receptor,epidermal growth factor%1-Phosphatidylinositol 3-kinase%Protein-serine-threonine kinases%Signal transduction%Disease models,animal
目的 探讨磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶蛋白(mTOR)信号转导通路与Barrett食管发生的关系.方法 将140只大鼠分为假手术组10只、铁剂组10只、食管十二指肠端侧吻合组30只、食管十二指肠端侧吻合加铁剂组30只、食管胃十二指肠侧侧吻合组30只、食管胃十二指肠侧侧吻合加铁剂组30只.最后共获得10份正常食管组织、62份反流性食管炎组织、34份Barrett食管组织,应用免疫组织化学方法检测以上3种组织中表皮生长因子受体(EGFR)、Akt、磷酸化Akt和磷酸化mTOR蛋白的表达水平.采用单因素方差分析、SNK两两比较和非参数相关性分析进行统计学处理.结果 Barrett食管组织中EGFR、Akt、磷酸化Akt、磷酸化mTOR蛋白的表达水平高于反流性食管炎和正常的食管组织(EGFR为0.1799±0.0367比0.0438±0.0025和0.0277±0.0069,q=6.79、4.13; Akt为0.1874±0.0250比0.0986±0.0093和0.0383±0.0048,q=6.51、3.56;磷酸化Akt为0.1418±0.0130比0.0592±0.0027和0.0281±0.0017,q=7.68、3.99;磷酸化mTOR为0.1591±0.0275比0.0674±0.0059和0.0112±0.0017,q=5.62、4.11,P均＜0.05).反流性食管炎食管组织中EGFR、Akt、磷酸化Akt、磷酸化mTOR蛋白的表达水平高于正常食管组织(q=4.67、4.29、4.27、4.03,P均＜0.05).结论 反流性食管炎、Barrett食管组织中PI3K/Akt/mTOR信号转导通路被激活,为临床多靶点治疗疾病提供了一定的理论依据.
目的 探討燐脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/哺乳動物雷帕黴素靶蛋白(mTOR)信號轉導通路與Barrett食管髮生的關繫.方法 將140隻大鼠分為假手術組10隻、鐵劑組10隻、食管十二指腸耑側吻閤組30隻、食管十二指腸耑側吻閤加鐵劑組30隻、食管胃十二指腸側側吻閤組30隻、食管胃十二指腸側側吻閤加鐵劑組30隻.最後共穫得10份正常食管組織、62份反流性食管炎組織、34份Barrett食管組織,應用免疫組織化學方法檢測以上3種組織中錶皮生長因子受體(EGFR)、Akt、燐痠化Akt和燐痠化mTOR蛋白的錶達水平.採用單因素方差分析、SNK兩兩比較和非參數相關性分析進行統計學處理.結果 Barrett食管組織中EGFR、Akt、燐痠化Akt、燐痠化mTOR蛋白的錶達水平高于反流性食管炎和正常的食管組織(EGFR為0.1799±0.0367比0.0438±0.0025和0.0277±0.0069,q=6.79、4.13; Akt為0.1874±0.0250比0.0986±0.0093和0.0383±0.0048,q=6.51、3.56;燐痠化Akt為0.1418±0.0130比0.0592±0.0027和0.0281±0.0017,q=7.68、3.99;燐痠化mTOR為0.1591±0.0275比0.0674±0.0059和0.0112±0.0017,q=5.62、4.11,P均＜0.05).反流性食管炎食管組織中EGFR、Akt、燐痠化Akt、燐痠化mTOR蛋白的錶達水平高于正常食管組織(q=4.67、4.29、4.27、4.03,P均＜0.05).結論 反流性食管炎、Barrett食管組織中PI3K/Akt/mTOR信號轉導通路被激活,為臨床多靶點治療疾病提供瞭一定的理論依據.
목적 탐토린지선기순3격매(PI3K)/단백격매B(Akt)/포유동물뢰파매소파단백(mTOR)신호전도통로여Barrett식관발생적관계.방법 장140지대서분위가수술조10지、철제조10지、식관십이지장단측문합조30지、식관십이지장단측문합가철제조30지、식관위십이지장측측문합조30지、식관위십이지장측측문합가철제조30지.최후공획득10빈정상식관조직、62빈반류성식관염조직、34빈Barrett식관조직,응용면역조직화학방법검측이상3충조직중표피생장인자수체(EGFR)、Akt、린산화Akt화린산화mTOR단백적표체수평.채용단인소방차분석、SNK량량비교화비삼수상관성분석진행통계학처리.결과 Barrett식관조직중EGFR、Akt、린산화Akt、린산화mTOR단백적표체수평고우반류성식관염화정상적식관조직(EGFR위0.1799±0.0367비0.0438±0.0025화0.0277±0.0069,q=6.79、4.13; Akt위0.1874±0.0250비0.0986±0.0093화0.0383±0.0048,q=6.51、3.56;린산화Akt위0.1418±0.0130비0.0592±0.0027화0.0281±0.0017,q=7.68、3.99;린산화mTOR위0.1591±0.0275비0.0674±0.0059화0.0112±0.0017,q=5.62、4.11,P균＜0.05).반류성식관염식관조직중EGFR、Akt、린산화Akt、린산화mTOR단백적표체수평고우정상식관조직(q=4.67、4.29、4.27、4.03,P균＜0.05).결론 반류성식관염、Barrett식관조직중PI3K/Akt/mTOR신호전도통로피격활,위림상다파점치료질병제공료일정적이론의거.
Objective To explore the relationship between phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammals target protein rapamycin (mTOR) signal transduction pathway and Barrett esophagus genesis.Methods A total of 140 rats were divided into sham operated group (n=10),iron group (n =10),esophageal duodenal side anastomosis group (n =30),esophageal duodenal side anastomosis plus iron group (n-30),esophageal gastric duodenal side anastomosis group (n=30) and esophageal gastric duodenal anastomosis plus iron group (n=30).In the end,10 normal esophagus tissue specimens,62 reflux esophagitis tissue specimens and 34 Barrett's esophagus tissue specimens were obtained.The expression levels of epidermal growth factor receptor (EGFR),Akt,phospho Akt (p-Akt),phospho-mTOR (p-mTOR) protein were detected by immunohistochemistry.Single factor analysis of variance,SNK between two groups and nonparametric correlation analysis were performed for statistical analysis.Results The protein expression levels of EGFR,Akt,p-Akt,p-mTOR in Barret(s esophagus tissues were higher than those in reflux esophagitis tissues and normal esophagus tissues (EGFR 0.1799±0.0367 vs 0.0438±0.0025 and 0.0277±0.0069,q=6.79,4.13; Akt 0.1874±0.0250 vs 0.0986±0.0093 and 0.0383±0.0048,q=6.51,3.56; p-Akt 0.1418±0.0130 vs 0.0592±0.0027 and 0.0281 ±0.0017,q=7.68,3.99; p-mTOR 0.1591±0.0275 vs 0.0674 ±0.0059 and 0.0112±0.0017,q=5.62,4.11; all P＜0.05).The protein expression levels of EGFR,Akt,p-Akt,and p-mTORin reflux esophagitis tissues were higher than those in normal esophagus tissues(q=4.67,4.29,4.27,4.03; all P＜0.05).Conclusion PI3K/Akt/mTOR signal transduction pathway were activated in reflux esophagitis and Barrett's esophagus,which provided theoretical basis for clinical multi-target treatment for diseases.
