中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2010年
7期
900-901,后插1
,共3页
肝脏%缺血%再灌注损伤%免疫原性
肝髒%缺血%再灌註損傷%免疫原性
간장%결혈%재관주손상%면역원성
Liver%Ischemia%Reperfusion injury%Immunogenicity
目的 观察缺血再灌注损伤对肝脏免疫原性的影响.方法 30只大鼠均分为3组,利用免疫荧光及Western blol检测缺血30min再灌注组及缺血60min再灌注组及对照组的肝脏中共刺激分子B7蛋白的表达水平.结果 正常肝脏B7-1、B7-2表达处于极低水平(0.035±0.005、0.025±0.004),缺血再灌注后肝脏B7-1、B7-2的蛋白表达明显升高(P<0.01),缺血再灌注60min组的B7-1、B7-2的表达水平明显高于缺血30min再灌注组(B7-1:0.070±0.017比0.051±0.008,B7-2:0.042±0.004.比0.037±0.004,P<0.01).结论 缺血再灌注损伤使共刺激分子B7蛋白表达升高,提示缺血再灌注损伤可使移植肝免疫原性升高,这些均能促进急性排斥反应的发生.
目的 觀察缺血再灌註損傷對肝髒免疫原性的影響.方法 30隻大鼠均分為3組,利用免疫熒光及Western blol檢測缺血30min再灌註組及缺血60min再灌註組及對照組的肝髒中共刺激分子B7蛋白的錶達水平.結果 正常肝髒B7-1、B7-2錶達處于極低水平(0.035±0.005、0.025±0.004),缺血再灌註後肝髒B7-1、B7-2的蛋白錶達明顯升高(P<0.01),缺血再灌註60min組的B7-1、B7-2的錶達水平明顯高于缺血30min再灌註組(B7-1:0.070±0.017比0.051±0.008,B7-2:0.042±0.004.比0.037±0.004,P<0.01).結論 缺血再灌註損傷使共刺激分子B7蛋白錶達升高,提示缺血再灌註損傷可使移植肝免疫原性升高,這些均能促進急性排斥反應的髮生.
목적 관찰결혈재관주손상대간장면역원성적영향.방법 30지대서균분위3조,이용면역형광급Western blol검측결혈30min재관주조급결혈60min재관주조급대조조적간장중공자격분자B7단백적표체수평.결과 정상간장B7-1、B7-2표체처우겁저수평(0.035±0.005、0.025±0.004),결혈재관주후간장B7-1、B7-2적단백표체명현승고(P<0.01),결혈재관주60min조적B7-1、B7-2적표체수평명현고우결혈30min재관주조(B7-1:0.070±0.017비0.051±0.008,B7-2:0.042±0.004.비0.037±0.004,P<0.01).결론 결혈재관주손상사공자격분자B7단백표체승고,제시결혈재관주손상가사이식간면역원성승고,저사균능촉진급성배척반응적발생.
Objective To investigate the effect of ischemia/reperfusion (I/R) injury on immunogenicity of the liver. Methods Thirty rats were randomly divided into three groups. The levels of B7 were assayed by using immunochemistry and Western blotting in the 30 min I/R group, 60-min I/R group, and control group. Results The levels of B7-1 and B7-2 were very low in normal liver tissues (0.035 ± 0. 005, 0. 025 ± 0. 004) , but markedly increased after I/R injury ( P < 0.01). The levels of B7-1 and B7-2 in the 60 min I/R group were higher than those in the 30 min I/R group (B7-1:0. 070 ± 0. 017 vs 0. 051 ± 0. 008, B7-2:0. 042 ± 0.004 vs 0. 037 ± 0.004; both P<0.01). Conclusion I/R injury increased the immunogenicity of the liver by up-regulating the costimulatory molecule B7, promoting the development of acute rejection.