Hughes C B, Gaber L W, Kotb M, Mohey el-Din A B, Pabst M, Gaber A O
Department of Surgery, University of Tennessee, Memphis 38163.
Surgery. 1995 Feb;117(2):201-5. doi: 10.1016/s0039-6060(05)80086-8.
Tumor necrosis factor-alpha (TNF-alpha) has been implicated as a mediator of the systemic manifestations associated with acute pancreatitis. The purpose of this study was to show that TNF-alpha expression in pancreatitis is a primary response and is not the result of endotoxemia.
Severe acute pancreatitis was induced in germ-free rats, which have no source of endogenous endotoxin, by ductal infusion of artificial bile. Control animals underwent sham operation and ductal infusion of saline solution. TNF-alpha levels were measured by the WEHI bioassay. Endotoxin was measured by the Limulus assay.
TNF-alpha levels remained low in the sham group (mean, 24.6 +/- 8.0 pg/ml) but were significantly elevated in normal rats with pancreatitis (181 +/- 26.8 pg/ml; p < 0.001 versus sham group) and in germ-free rats with pancreatitis (213 +/- 90 pg/ml; p < 0.002 versus sham group). No endotoxin was detected in any of the experimental rats.
Our results indicate that TNF-alpha levels are elevated in acute pancreatitis despite the absence of endotoxin, indicating a primary role of TNF-alpha in this disease.
肿瘤坏死因子-α（TNF-α）被认为是与急性胰腺炎相关的全身表现的介质。本研究的目的是表明胰腺炎中TNF-α的表达是一种原发性反应，而非内毒素血症的结果。
通过导管输注人工胆汁在无内源性内毒素来源的无菌大鼠中诱导重症急性胰腺炎。对照动物接受假手术并导管输注盐溶液。通过WEHI生物测定法测量TNF-α水平。通过鲎试剂测定法测量内毒素。
假手术组中TNF-α水平保持较低（平均24.6±8.0 pg/ml），但在患有胰腺炎的正常大鼠中显著升高（181±26.8 pg/ml；与假手术组相比，p<0.001），在患有胰腺炎的无菌大鼠中也显著升高（213±90 pg/ml；与假手术组相比，p<0.002）。在任何实验大鼠中均未检测到内毒素。
我们的结果表明，尽管不存在内毒素，但急性胰腺炎中TNF-α水平仍会升高，这表明TNF-α在该疾病中起主要作用。
