阻塞性黄疸肠粘膜屏障功能损害的机制及丹参保护作用

Mechanism of injury of enteromucosal barrier in obstructive jaundice

目的 :观察阻塞性黄疸 (阻黄 )时肠粘膜屏障功能损害与中性粒细胞 (PMN)的关系及丹参的保护作用。方法 :SD大鼠 48只分为 4组 :假手术对照组 (SO+NS)、阻黄组 (BDL +NS)、治疗对照组 (SO+SM)及丹参治疗组 (BDL+SM) ,于胆管结扎第 7、1 4天两个时相点分别检测门静脉内毒素、小肠髓过氧化酶 (MPO)和小肠二胺氧化酶 (DAO)活性 ,观察肠粘膜结构变化。结果 :BDL+NS组第 7、1 4天两时相点 ,内毒素逐渐增高 [(1 .0 77± 0 .336) Eu/ m L→ (2 .1 85± 0 .566) Eu/ m L ,P<0 .0 1 ] ,小肠 MPO活性升高 [(2 .850± 1 .2 2 0 ) U/ mg→(4.92 9± 1 .371 ) U/ mg,P<0 .0 1 ] ,小肠 DAO活性逐渐下降 [(1 .70 3± 0 .355) U/ mg→ (1 .2 1 8± 0 .40 7) U/ mg,P<0 .0 5] ,肠粘膜损伤评分升高。 BDL+SM组第 7天时与 BDL+NS组比较内毒素降低和 DAO活性升高均很显著 ,基本接近 SO+SM组水平 ,第 1 4天时与 BDL+NS组比较内毒素显著降低和 DAO活性显著升高 ,但与 SO+SM组差异仍有显著性 ,而 BDL+SM组的 MPO活性却逐日增高 ,第 7、1 4天时与 BDL +NS组差异无显著性 (P>0 .0 5)。结论 :PMN聚集并活化是阻黄时肠粘膜屏障功能损害的重要机制 ;丹参能早期保护肠粘膜屏障功能 ,但不是通过阻止 PMN聚集来实现的。

Objective: To investigate the relationship between the change of polymorphonuclear neutrophils(PMNs) and the degree of injury of enteromucosal barrier,and the protective effect of salvia miltiorrhiza(SM) in obstructive jaundice Methods: Intestinal activities of diamine oxidase(DAO) and myeloperioxidase(MPO),plasma endotoxin level in portal vein and the enteromucosal histology were examined on the 7th and 14th days,respectively Results: In bile duct ligation(BDL) group,intestinal DAO activity was decreased from(1 703±0 355) U/mg to (1 218±0 407)U/mg on the 14th day( P <0 05),whereas intestinal MPO activity and plasma endotoxin level in portal vein were significantly increased(2 850±1 220 U/mg vs 4 929±1 371 U/mg;1 077±0 336 Eu/mL vs 2 185±0 566 Eu/mL; P <0 01) There were obvious enteromucosal histological changes on the 14th day In comparison with BDL plus normal saline(NS) group,intestinal DAO activity or plasma endotoxin level in BDL+SM group was remarkably increased or decreased( P <0 01),whereas intestinal MPO activity showed no significant difference( P >0 05) Conclusion: Injury of enteromucosal barrier could mainly result from aggregation of activated PMNs in intestinal tissue in obstructive jaundice,SM may have an early protective effect on enteromucosal barrier without inhibiting aggregation of PMNs