目的探討大鼠阻塞性黃疸小腸組織中細(xì)胞間粘附分子-1（ICAM-1）和腫瘤壞死因子-α（TNF-α）的表達(dá)及意義。方法選SD大鼠24只，用隨機(jī)排列表法均分成假手術(shù)組（SO組）和阻塞性黃疸組（BDL組），每組術(shù)后再隨機(jī)分設(shè)7 d和14 d兩個時相點。應(yīng)用免疫組化的方法觀察小腸組織中ICAM-1表達(dá)的變化，采用雙抗體夾心ELISA法測定TNF-α含量，同時檢測小腸組織中髓過氧化物酶（MPO）活性、小腸組織和血漿中二胺氧化酶（DAO）活性。結(jié)果膽總管結(jié)扎后7 d、14 d，ICAM-1表達(dá)主要在小腸粘膜上皮細(xì)胞，且表達(dá)逐漸增強(qiáng)（P＜0.05）； 小腸粘膜TNF-α的含量逐漸上升，分別為（14.25±1.01） ng/g和（23.83±1.43） ng/g（P＜0.01）； 小腸DAO的活性逐漸降低，分別為（1.70±0.36） U/mg和（1.22±0.41） U/mg（P＜0.01）； 血漿DAO活性逐漸升高，分別為（6.44±1.74） U/ml和（8.93±1.29） U/ml（P＜0.01）； MPO活性逐漸增高，分別為（2.85±1.22 ） U/mg和（4.93±1.37） U/mg（P＜0.01）。結(jié)論阻塞性黃疸時小腸組織的ICAM1表達(dá)顯著上調(diào)和小腸粘膜TNFα含量顯著升高, 參與了中性粒細(xì)胞介導(dǎo)的小腸粘膜損傷。
引用本文： 繆輝來,林木生,陳明,陳念平,包仕廷. 大鼠阻塞性黃疸小腸組織中細(xì)胞間粘附分子-1和腫瘤壞死因子-α的表達(dá)及其意義. 中國普外基礎(chǔ)與臨床雜志, 2004, 11(4): 331-334. doi: 復(fù)制
版權(quán)信息： ?四川大學(xué)華西醫(yī)院華西期刊社《中國普外基礎(chǔ)與臨床雜志》版權(quán)所有，未經(jīng)授權(quán)不得轉(zhuǎn)載、改編
| 1. | Wang X, Sun Z, Borjesson A, et al. Inhibition of plateletactivating factor, intercellular adhesion molecule 1 and platelet endothelial cell adhesion molecule 1 reduces experimental pancreatitisassociated gut endothelial barrier dysfunction [Ｊ]. Br J Surg， 1999; 86(3)∶ 411. |
| 2. | Jackson GD, Dai Y, Sewell WA. Bile mediates intestinal pathology in endotoxemia in rats [Ｊ]. Infect Immun， 2000; 68(8)∶4714. |
| 3. | Wardle EN, Wright NA. Endotoxin and acute renal failure associated with obstructive jaundice [Ｊ]. Br Med J， 1970; 4(733)∶472. |
| 4. | Kubes P, Arfors KE, Granger DN. Plateletactivating factorinduced mucosal dysfunction: role of oxidants and granulocytes [Ｊ]. Am J Physiol， 1991; 260(6 Pt 1)∶G965. |
| 5. | Moore EE, Moore FA, Franciose RJ, et al. The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure [Ｊ]. J Trauma, 1994; 37(6)∶881. |
| 6. | Wang X, Andersson R. The role of endothelial cells in the systemic inflammatory response syndrome and multiple system organ failure [Ｊ]. Eur J Surg, 1995; 161(10)∶703. |
| 7. | Essani NA, Fisher MA, Farhood A, et al. Cytokineinduced upregulation of hepatic intercellular adhesion molecule1 messenger RNA expression and its role in the pathophysiology of murine endotoxin shock and acute liver failure [Ｊ]. Hepatology, 1995; 21(6)∶1632. |
- 1. Wang X, Sun Z, Borjesson A, et al. Inhibition of plateletactivating factor, intercellular adhesion molecule 1 and platelet endothelial cell adhesion molecule 1 reduces experimental pancreatitisassociated gut endothelial barrier dysfunction [Ｊ]. Br J Surg， 1999; 86(3)∶ 411.
- 2. Jackson GD, Dai Y, Sewell WA. Bile mediates intestinal pathology in endotoxemia in rats [Ｊ]. Infect Immun， 2000; 68(8)∶4714.
- 3. Wardle EN, Wright NA. Endotoxin and acute renal failure associated with obstructive jaundice [Ｊ]. Br Med J， 1970; 4(733)∶472.
- 4. Kubes P, Arfors KE, Granger DN. Plateletactivating factorinduced mucosal dysfunction: role of oxidants and granulocytes [Ｊ]. Am J Physiol， 1991; 260(6 Pt 1)∶G965.
- 5. Moore EE, Moore FA, Franciose RJ, et al. The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure [Ｊ]. J Trauma, 1994; 37(6)∶881.
- 6. Wang X, Andersson R. The role of endothelial cells in the systemic inflammatory response syndrome and multiple system organ failure [Ｊ]. Eur J Surg, 1995; 161(10)∶703.
- 7. Essani NA, Fisher MA, Farhood A, et al. Cytokineinduced upregulation of hepatic intercellular adhesion molecule1 messenger RNA expression and its role in the pathophysiology of murine endotoxin shock and acute liver failure [Ｊ]. Hepatology, 1995; 21(6)∶1632.