摘要
目的 探讨雷公藤多甙对大鼠急性坏死性胰腺炎 (ANP)的免疫调节作用。方法 将6 0只牛磺胆酸钠诱导的ANP大鼠分成不治疗组、雷公藤多甙组和橄榄油对照组共 3组 ,另取 6只正常大鼠作为对照组。每组分别在术后 6和 12h各处死 6只大鼠取血 ,测淀粉酶、内毒素、TNF α和IL 1水平 ,观察胰腺组织的病理变化。结果 雷公藤组有 3只动物生存 3d以上 ,不治疗组及橄榄油对照组大鼠 3d内全部死亡。不治疗组与雷公藤组 12h后血清淀粉酶、内毒素、TNF α和IL 1水平分别为34 116U/ml、1 42 83EU/ml、34 6pg/ml和 2 17pg/ml及 10 2 2 0U/ml、0 145 6EU/ml、2 0 0pg/ml和 147pg/ml(P值均小于 0 0 5 )。两组光学显微镜病理学的水肿、炎症、出血和坏死评分分别为 3 0 0、3 2 8、2 89和 2 6 7及 2 39、2 0 6、1 0 0和 0 84(P值均小于 0 0 5 )。结论 雷公藤的免疫调节效应已初步显示对ANP大鼠有一定的保护作用 ,其机理值得进一步探讨。
Objective[WT5”BZ] We investigated the immunoregulatory effect of TII an extract of Tripterygium wilfordii Hook F in rats with acute necrotizing pancreatitis (ANP).[WT5”HZ]Methods[WT5”BZ] 60 ANP rats induced by injection of sodium taurocholate into the pancreatic duct were divided into 3 groups: untreated group, TII treated group, and oliver oil control group. Another 6 normal rats were used as contral group. At 6 and 12 hours after the induction of ANP 6 rats in each group were sacrificed and blood samples were taken for the measurement of serum amylase, endotoxin, IL 1 and TNF α level were measured, and pathological study of pancreas was performed. [WT5”HZ]Results[WT5”BZ] 3 rats of TII treated group survived for longer than 3 days. No rat in untreated group lived for more than 3 days. At 12 hours, TII group's serum amylase, endotoxin, IL 1 and TNF α level were significantly lower than that of untreated group: 10?220?U/ml, 0 145?6 EU/ml, 200?pg/ml and 147?pg/ml v s.34?116?U/ml, 1 4?283?EU/ml, 346?pg/ml and 217 pg/ml respectively (all P <0 05). Pathological scores of pancreatic edema, inflammation,hemorrhage and necrosis were all less severe in TII group than that of untreated group: 2 39, 2 06, 1 00 and 0 84 v s. 3 00, 3 28, 2 89 and 2 67 respectively (all P <0 05).[WT5”HZ]Conclusion[WT5”BZ] TII's positive immunoregulatory effect on murid ANP model may have clinical implication. [WT5”HZ]
出处
《中华普通外科杂志》
CSCD
2000年第5期283-285,共3页
Chinese Journal of General Surgery
关键词
急性坏死性胰腺炎
雷公藤多甙
免疫调节效应
WT5”BZ] Pancreatitis
Triptolide Hook F
Tumor necrosis factor
Interleukin 1