大鼠实验性胃溃疡自愈期间胃黏膜组织凋亡相关因子bax,bcl2的表达变化

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1、大鼠实验性胃溃疡自愈期间胃黏膜组织凋亡相关因子Bax,Bcl2的表达变化作者：张静陈丽薇吕洋吴靖芳【摘要】目的：探讨大鼠实验性胃溃疡自愈期间促凋亡蛋白Bax与抗凋亡蛋白Bcl2在胃黏膜组织中表达的变化。方法：胃前壁黏膜下注射冰乙酸制备大鼠胃溃疡模型，免疫组织化学法检测正常组、溃疡组、盐水组大鼠胃黏膜组织Bax和Bcl2表达变化,并应用图像分析系统软件进行积分光密度值(IOD)分析。结果：Bax阳性细胞在胃溃疡组1d即增多，表达强度强，显著高于正常组与相应盐水组(P<0.01);之后随术后时间延长,阳性细胞逐渐减少,表达强度渐弱,

2、至术后23d，溃疡组BaxIOD与对照组相比差异无统计学意义(P>0.05)。Bcl2阳性细胞随术后时间延长表达逐渐增多,至胃溃疡损伤后的第6天Bcl2阳性细胞数量最多，表达强度最强，胃溃疡损伤后10d及14dBcl2IOD略低于溃疡后6d，但仍维持于较高水平，至胃溃疡损伤后23d，Bcl2IOD显著降低，与正常组、盐水组相比差异无统计学意义(P>0.05)。结论:大鼠胃溃疡自愈期间Bax与Bcl2共同参与了胃黏膜的损伤修复。在胃溃疡损伤早期以促凋亡因素为主，抗凋亡因素对溃疡胃黏膜的保护及修复作用主要是在损伤后的6～1

3、4d。【关键词】胃溃疡;Bcl2;Bax;免疫组织化学;大鼠10　　【ABSTRACT】Objective:ToinvestigatetheexpressionofBaxandBcl2proteinsingastricmucosaduringselfhealingofexperimentalgastriculcerinrats.Methods:Aceticacidinducedulcerswerecausedbyinjectionaceticacidtosubmucosalofpariesanteriorgastricus.Thee

4、xpressionsofBaxandBcl2ingastriculcergroup(GU),normalsalinegroup(NS)andnormalgroup(N)weredetectedbyimmunohistochemicalmethod,andtheresultsofIODwereanalyzedbyusingtheimageanalyticalsystems.Results:Baxpositivecellssignificantlyincreasedandshowedstrongexpressiononthefirstdaya

5、ftertheexperimentalgastriculcerinrats,theIODvaluewasmarkedlyhigherthanthatincontrolgroups(P<0.01).ThentheIODvaluesofBaxcellsinGUgroupweregraduallydecreased,andon23rdday，whichhadnotstatisticaldifferencecomparedwiththatofthecontrolgroups(P>0.05).TheexpressionofBcl2gra

6、duallyincreasedandtheIODofBcl2reachedthepeak(IOD=21.038±7.537)onthe6thdayinGUgroup,whichshowedthereductiontendency,butonthe10thand14thdays,theIODvaluesstillstayedatthehigherlevel.Onthe23thdayinGUgroup,IODdecreasedsignificantly,andhadnostatisticaldifferencecomparedwith10th

7、atofcontrolgroups(P>0.05).Conclusion:BaxandBcl2proteinsparticipateinrenovatingthegastricmucosaduringhealingofexperimentalgastriculcerinrats.TheproapoptosisproteinBaxplaysmainroleintheearlystageoftheexperimentalgastriculcer,andantiapotosisproteinbcl2protectsandrepair

8、sstomachmucosaon6～14daftertheexperimentalgastriculcerinrats.　　【KEYWORDS】Stomachulcer,Bax,