摘要
目的研究活性氧对肝癌缺血再灌注(I/R)后的损伤作用。方法建立兔肝脏肿瘤模型,并于肝缺血再灌注和经门静脉穿刺一次性灌注高氧液(氧分压为80kPa)5 mL后1 h,1 d,3 d和7 d各时点分别取肿瘤组织和肝脏组织,测定超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的含量。用TUNEL染色法观察组织的细胞凋亡情况。结果单纯I/R后正常肝组织和肝癌组织中的SOD浓度均有明显下降,正常肝脏组织CAT浓度均有所升高,肝癌组织中于再灌注1 d CAT浓度显著降低并达最低水平。恢复血流同时经门静脉灌注高氧液后,正常肝组织及肝癌组织中SOD浓度均较I/R各个时点明显降低,但再灌注7 d时仍低于再灌注前。两种组织中的CAT浓度于I/R 1 h下降达最低,但从再灌注3 d以后,正常肝组织中的CAT浓度回升至正常水平,而再灌注7 d时肝癌组织中的CAT浓度仍处于较低水平。I/R后正常肝组织和肝癌组织的凋亡细胞增多,肝癌组织中细胞凋亡在灌注高氧液后1 d和3 d最为显著。I/R和灌注高氧液后,肝癌组织中SOD和CAT的浓度和凋亡细胞改变均较正常肝组织显著(P<0.01)。结论经门静脉灌注高氧液可加强I/R对肝癌组织的氧化改变和损伤,而对正常肝脏组织的影响较小。
Objective To study the injurious effect of active oxygen on hepatocarcinoma after ischemia and reperfusion. Methods The models of ischemia and reperfusion ( I/R ) of hepatocarcinoma were established. The model was reperfued alone or combination with perfued with hyperoxic fluid (Partial pressure of oxygen, PO2 〉 80) via portal vein. After reperfusion 1 h, 1 d, 3d and 7 d respectively, the concentration of superoxide dismutase ( SOD ) and catalase ( CAT ) were tested, and the apoptosis of hepatocarcinoma also was observed using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method. Results The results indicated that the SOD concentration in both hepatocarcinoma tissue and normal hepatic tissues decreased following I/R and perfusion with hyperoxic fluid liquid. The concentration of CAT increased following I/R in normal hepatic tissues. In hepatocarcinoma tissue, concentration of CAT decreased after reperfusion for 1 d and reached its lowest point. After perfusion with hyperoxic fluid, the concentration of SOD in both hepatocarcinoma tissue and normal hepatic tissues decreased more quickly following I/R and the low level was still found on 7 d after reperfusion. The concentration of CAT in tissues of both groups decreased and reached the lowest level at 1 h after reperfusion, but it was restored at 3 d reperfusion in normal hepatic tissues, and in hepatocarcinoma tissue was still at lower level until 7 d after reperfusion. After I/R, the apoptotic ceils increased in normal hepatic and hepatic cancer tissues, and were most marked in tissues of hepatic carcinoma at 1 d and 3 d after perfusion with hyperoxic fluid. After I/R and perfusing with hyperoxic fluid, the changes of SOD and CAT and apoptosis in hepatocarcinoma tissue were more obvious than that in normal hepatic tissues ( P 〈 0.01 ). Conclusions Perfusion with hyperoxic fluid via portal vein can intensify hepatio ischemia and reperfusion injury, but has less effect on normal hepatic tissues.
出处
《中国普通外科杂志》
CAS
CSCD
2008年第1期25-28,共4页
China Journal of General Surgery
关键词
肝肿瘤
缺血再灌注损伤
超氧化物歧化酶
高氧液
活性氧
Liver Neoplasms
Ischemia-reperfusion Injury
Super-oxide Dismutase
Hyperoxia Liquid
Oxygen Radical