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肿瘤坏死因子(TNFa)是急性胰腺炎导致全身多器官损害的一种重要介质。本文研究的目的是了解慢性酒精性胰腺炎TNFa和可溶性肿瘤坏死因子受体p55、p75(sTNFRp55、sTNFRp75)是否升高,及其升高是否是内毒素或酒精的作用。我们对12例慢性酒精性胰腺炎患者和8例健康者用内毒素脂多糖(LPS)和乙醇(Ethanol)刺激后的周围血单核细胞上清液用ELISA方法进行了TNFa、sTNFRp55、p75的检测。LPS刺激后的单核细胞上清液中TNFa、sTNFp55、p75浓度不论是患者还是健康组均较自然表达明显增加,其中sTNFRp55、p75浓度在胰腺炎组较正常组明显增加,P值分别<0.05、<0.001。Ethanol刺激后 TNFa和sTNFRp55的表达在胰腺炎组与正常组之间无差异.但sTNFRp75较正常组增加。我们的结果提示慢性酒精性胰腺炎前炎性介质TNFa和sTNFRp55、p75的诱导与内毒素活化的单核细胞表达有关,而酒精对单核细胞活化不起直接作用。
Tumor necrosis factor (TNFa) is an important mediator of multiple organ damage in acute pancreatitis. The purpose of this study is to investigate whether elevated serum TNFa and soluble tumor necrosis factor receptors p55, p75 (sTNFRp55, sTNFRp75) and their elevation are endotoxin or alcohol. In 12 patients with chronic alcoholic pancreatitis and 8 healthy individuals, peripheral blood mononuclear cell supernatant stimulated by lipopolysaccharide (LPS) and alcohol (Ethanol) was used to detect TNFa, sTNFRp55, p75 Detection. The concentrations of TNFa, sTNFp55 and p75 in mononuclear cell supernatant stimulated by LPS were significantly higher than those in healthy patients or healthy individuals, and the concentrations of sTNFRp55 and p75 in pancreatitis group were significantly higher than those in normal group (P <0.05) , <0.001. The expression of TNFa and sTNFRp55 did not differ between the pancreatitis group and the normal group after Ethanol stimulation, but sTNFRp75 increased compared with the normal group. Our results suggest that the induction of TNFa and sTNFRp55, p75 by pro-inflammatory mediators of chronic alcoholic pancreatitis is associated with the expression of endotoxin-activated monocytes, whereas alcohol has no direct effect on monocyte activation.