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己酮可可碱治疗大鼠实验性急性胰腺炎的有益作用。

Beneficial effects of pentoxifylline treatment of experimental acute pancreatitis in rats.

作者信息

Marton J, Farkas G, Takacs T, Nagy Z, Szasz Z, Varga J, Jarmay K, Balogh A, Lonovics J

机构信息

Department of Surgery, Albert Szent-Gyorgyi Medical University, Szeged, Hungary.

出版信息

Res Exp Med (Berl). 1998;197(5):293-9. doi: 10.1007/s004330050078.

DOI:10.1007/s004330050078
PMID:9561559
Abstract

UNLABELLED

The purposes of this study were to determine the tumor necrosis factor (TNF) and interleukin-6 (IL-6) levels after the induction of acute necrotizing pancreatitis, and to establish the effects of pentoxifylline on cytokine production.

METHODS

acute pancreatitis was induced by the retrograde injection of 200 microliters taurocholic acid into the pancreatic duct in male Wistar rats. The serum amylase activity, the wet pancreatic weight/body weight ratio, and the TNF and IL-6 levels were measured. Seven mg/kg pentoxifylline were administered intraperitoneally at the time of operation 6, 12 or 24 h later. Rats were killed 6, 24, 48 or 72 h after the operation.

RESULTS

the TNF bioassay revealed high levels of TNF (30.2 +/- 5.4 U/ml, 35.0 +/- 5.0 U/ml and 36.6 +/- 6.0 U/ml) in the control group at 6, 24 and 48 h and (54.1 +/- 20 U/ml and 10.9 +/- 4.2 U/ml) in the pentoxifylline-treated group at 6 and 24 h, respectively, whereas the level had decreased to zero in the pentoxifylline-treated group at 48 h. The IL-6 bioassay likewise demonstrated high levels of IL-6 in the control group at 48 h and in the pentoxifylline-treated group at 6 and 24 h, and markedly decreased levels in the pentoxifylline-treated group at 48 h (7083 +/- 2844 pg/ml, 6463 +/- 1307 pg/ml, 10,329 +/- 5571 pg/ml vs 137.5 +/- 85.5 pg/ml, respectively, P < 0.05). The high mortality observed in the pancreatitis group (43%) was decreased by pentoxifylline administration to 11%.

CONCLUSION

these results demonstrate that pentoxifylline very effectively inhibits cytokine production in acute pancreatitis.

摘要

未标记

本研究的目的是确定急性坏死性胰腺炎诱导后肿瘤坏死因子(TNF)和白细胞介素-6(IL-6)的水平,并确定己酮可可碱对细胞因子产生的影响。

方法

通过向雄性Wistar大鼠胰管逆行注射200微升牛磺胆酸诱导急性胰腺炎。测量血清淀粉酶活性、胰腺湿重/体重比以及TNF和IL-6水平。在手术时、6、12或24小时后腹腔注射7毫克/千克己酮可可碱。术后6、24、48或72小时处死大鼠。

结果

TNF生物测定显示,对照组在6、24和48小时时TNF水平较高(分别为30.2±5.4 U/ml、35.0±5.0 U/ml和36.6±6.0 U/ml),己酮可可碱治疗组在6和24小时时分别为(54.1±20 U/ml和10.9±4.2 U/ml),而己酮可可碱治疗组在48小时时该水平已降至零。IL-6生物测定同样显示,对照组在48小时时IL-6水平较高,己酮可可碱治疗组在6和24小时时较高,而己酮可可碱治疗组在48小时时水平显著降低(分别为7083±2844 pg/ml、6463±1307 pg/ml、10329±5571 pg/ml对137.5±85.5 pg/ml,P<0.05)。胰腺炎组观察到的高死亡率(43%)通过给予己酮可可碱降至11%。

结论

这些结果表明己酮可可碱非常有效地抑制急性胰腺炎中细胞因子的产生。

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