临床医学工程
臨床醫學工程
림상의학공정
CLINICAL MEDICAL ENGINEERING
2014年
5期
555-557
,共3页
炎症性肠病%环氧合酶-2%核转录因子-κb%儿茶素单体
炎癥性腸病%環氧閤酶-2%覈轉錄因子-κb%兒茶素單體
염증성장병%배양합매-2%핵전록인자-κb%인다소단체
Inflammatory bowel disease (IBD)%COX-2%NF-κB%Epigallocatechin gallate (EGCG)
目的：探索儿茶素单体表没食子儿茶素没食子酸酯(耘G悦G)在治疗炎症性肠病(陨月阅)模型大鼠作用中对晕云-κ月信号通路的影响。方法将36只健康杂阅大鼠随机分为正常对照组、模型组、耘G悦G治疗组，每组12只，以三硝基苯磺酸(栽晕月杂)灌肠制作大鼠陨月阅模型。灌肠用药2周后，分别用耘蕴陨杂A检测肠组织中孕G耘2、晕韵含量；免疫组化检测肠粘膜悦韵载-2、蚤晕韵杂的蛋白表达；宰藻泽贼藻则灶月造燥贼贼蚤灶早检测大鼠肠粘膜晕云-κ月责65蛋白水平的变化。结果①模型组肠组织内孕G耘2、晕韵含量显著增高。耘G悦G治疗组大鼠肠组织内孕G耘2、晕韵含量与模型组相比显著减少(孕越0.000)；②模型组肠粘膜组织中悦韵载-2表达明显增强，正常结肠组织未见或少见悦韵载-2蛋白表达。而耘G悦G灌肠后大鼠肠组织中悦韵载-2的表达显著下降。③模型组肠粘膜组织中蚤晕韵杂表达明显增强，正常结肠组织未见或少见蚤晕韵杂蛋白表达。而耘G悦G灌肠后大鼠肠组织中蚤晕韵杂的表达显著下降。④正常大鼠肠组织晕云-κ月责65蛋白水平较低，模型组肠组织内晕云-κ月责65蛋白水平显著增加。耘G悦G可显著抑制肠组织内晕云-κ月责65蛋白水平表达。结论耘G悦G可通过降低晕云-κ月责65蛋白的表达，下调悦韵载-2、蚤晕韵杂的表达，使其产物孕G耘2、晕韵生成减少，从而达到减轻炎症的目的。因此晕云-κ月可作为耘G悦G治疗大鼠实验性结肠炎的一个有效的分子“靶点”。
目的：探索兒茶素單體錶沒食子兒茶素沒食子痠酯(耘G悅G)在治療炎癥性腸病(隕月閱)模型大鼠作用中對暈雲-κ月信號通路的影響。方法將36隻健康雜閱大鼠隨機分為正常對照組、模型組、耘G悅G治療組，每組12隻，以三硝基苯磺痠(栽暈月雜)灌腸製作大鼠隕月閱模型。灌腸用藥2週後，分彆用耘蘊隕雜A檢測腸組織中孕G耘2、暈韻含量；免疫組化檢測腸粘膜悅韻載-2、蚤暈韻雜的蛋白錶達；宰藻澤賊藻則竈月造燥賊賊蚤竈早檢測大鼠腸粘膜暈雲-κ月責65蛋白水平的變化。結果①模型組腸組織內孕G耘2、暈韻含量顯著增高。耘G悅G治療組大鼠腸組織內孕G耘2、暈韻含量與模型組相比顯著減少(孕越0.000)；②模型組腸粘膜組織中悅韻載-2錶達明顯增彊，正常結腸組織未見或少見悅韻載-2蛋白錶達。而耘G悅G灌腸後大鼠腸組織中悅韻載-2的錶達顯著下降。③模型組腸粘膜組織中蚤暈韻雜錶達明顯增彊，正常結腸組織未見或少見蚤暈韻雜蛋白錶達。而耘G悅G灌腸後大鼠腸組織中蚤暈韻雜的錶達顯著下降。④正常大鼠腸組織暈雲-κ月責65蛋白水平較低，模型組腸組織內暈雲-κ月責65蛋白水平顯著增加。耘G悅G可顯著抑製腸組織內暈雲-κ月責65蛋白水平錶達。結論耘G悅G可通過降低暈雲-κ月責65蛋白的錶達，下調悅韻載-2、蚤暈韻雜的錶達，使其產物孕G耘2、暈韻生成減少，從而達到減輕炎癥的目的。因此暈雲-κ月可作為耘G悅G治療大鼠實驗性結腸炎的一箇有效的分子“靶點”。
목적：탐색인다소단체표몰식자인다소몰식자산지(운G열G)재치료염증성장병(운월열)모형대서작용중대훈운-κ월신호통로적영향。방법장36지건강잡열대서수궤분위정상대조조、모형조、운G열G치료조，매조12지，이삼초기분광산(재훈월잡)관장제작대서운월열모형。관장용약2주후，분별용운온운잡A검측장조직중잉G운2、훈운함량；면역조화검측장점막열운재-2、조훈운잡적단백표체；재조택적조칙조월조조적적조조조검측대서장점막훈운-κ월책65단백수평적변화。결과①모형조장조직내잉G운2、훈운함량현저증고。운G열G치료조대서장조직내잉G운2、훈운함량여모형조상비현저감소(잉월0.000)；②모형조장점막조직중열운재-2표체명현증강，정상결장조직미견혹소견열운재-2단백표체。이운G열G관장후대서장조직중열운재-2적표체현저하강。③모형조장점막조직중조훈운잡표체명현증강，정상결장조직미견혹소견조훈운잡단백표체。이운G열G관장후대서장조직중조훈운잡적표체현저하강。④정상대서장조직훈운-κ월책65단백수평교저，모형조장조직내훈운-κ월책65단백수평현저증가。운G열G가현저억제장조직내훈운-κ월책65단백수평표체。결론운G열G가통과강저훈운-κ월책65단백적표체，하조열운재-2、조훈운잡적표체，사기산물잉G운2、훈운생성감소，종이체도감경염증적목적。인차훈운-κ월가작위운G열G치료대서실험성결장염적일개유효적분자“파점”。
Objective To explore the effect of epigallocatechin gallate (EGCG) on NF-κB signal way of inflammatory bowel disease (IBD). Methods Twenty-four SD rats underwent enema of trinitrobenzene sulfonic acid (TNBS) to cause IBD and then randomly divided into two groups:model group, undergoing enema of normal saline (NS) once a day for 2 weeks;EGCG treated group, undergoing enema of 100 mg/kg EGCG;Another 12 rats were used as normal controls. Two weeks later the rats were killed. The levels of PGE2 and NO in gut were evaluated. The cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in the colonic mucosa was detected by immunohistochemistry. The NF-κB p65 expression was assessed by Western Blotting. Results EGCG could decrease COX-2 and iNOS protein expression as well as PGE2, NO content in colonic tissue. These beneficial effects of EGCG were associated with a significant reduction of NF-κB p65 activation. Conclusions Our data demonstrate that EGCG may be beneficial in colitis by decreasing COX-2 and iNOS as well as PGE2, NO content in colonic tissue. The NF-κB expression might construct the molecular base of EGCG regarding to its anti-inflammation effect.
