TNF-α在重症急性胰腺炎发病中的作用及人参二醇皂苷的治疗作用

Reseach of the mechanism of severe acute pancreatitis and the therapeutic effect of Panaxadiol Saponin

目的探讨TNF-α、COX-2在重症急性胰腺炎(SAP)发病中的作用及人参二醇皂苷对SAP的治疗作用。方法雄性SD大鼠120只,随机分为假手术组、SAP模型组、人参二醇皂苷干预组和地塞米松干预组,每组30只。除假手术组外,其他胰管内注射5%牛磺胆酸钠1 mg/kg,制备SAP大鼠模型。各组于术后6、12、24 h三个时间点各处死10只大鼠,腹主动脉取血检测血清TNF-a水平;取各组术后6 h处死大鼠的胰头组织行HE染色及免疫组化染色分别观察大鼠胰腺组织病理学变化及COX-2的表达情况。结果假手术组胰腺组织未见明显异常,模型组胰腺组织大片坏死,血管破裂出血,炎性细胞浸润,人参二醇皂苷干预组及地塞米松干预组可见炎性细胞浸润程度及坏死程度减轻。各时间点模型组大鼠血清TNF-α明显高于假手术组(P<0.01)和人参二醇皂苷干预组及地塞米松干预组(P<0.05)。模型组、人参二醇皂苷干预组和地塞米松干预组的COX-2阳性率分别为90%、60%和50%,假手术组阳性率为0,模型组COX-2阳性率高于两个干预组(P<0.05)。结论TNF-α介导了SAP的发生发展,且增加了COX-2在SAP中的表达活性;人参二醇皂苷可以减轻SAP的炎症反应。

Objective To investigate the role of TNF-α and COX-2 in the development of severe acute pancreatitis （SAP） and the therapeutic effect of Panaxadiol Saponin （PDS）. Methods 120 SD rats were randomly divided into sham operation group, SAP model group, PDS treated group and Dexamethasone treated group. There were 30 rats in each group. Rats in each group were killed 6, 12 and 24 h （ 10 rats for each time point） after operation to determine the serum levels of TNF-α. The pancreas tissues of the rats of 6 h after operation were obtained to conduct HE dye and immunohistochemistry assay to examine the changes with microscope and the expression of COX-2. Resets The pancreas tissues in sham operation group had no obvious changes. It could be seen in model group that pancreas tissue necrosis, blood vessel breach and bleeding and inflammation cell infiltration. The changes in PDS and Dexamethasone treated group were less than those of model group. Serum TNF-α levels in model group were higher than that in sham operation group（ P 〈0.01 ） and PDS and Dexamethasone treated group （P 〈0. 05）. The expression of COX-2 in model group,PDS and Dexamethasone treated group was 90% ,60% and 50% respectively. The expression of COX-2 in model group were higher than that of PDS and Dexamethasone treated group （ P 〈 0. 05 ）. Conclusions TNF-α induces the developing of SAP and increases the expression of COX-2, PDS can reduce the inflammation response of SAP.