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啮齿动物闭合十二指肠袢性胰腺炎中的氧化应激

Oxidative stress in rodent closed duodenal loop pancreatitis.

作者信息

Peralta J, Reides C, García S, Llesuy S, Pargament G, Carreras M C, Catz S, Poderoso J J

机构信息

Laboratory of Oxygen Metabolism, University Hospital, Buenos Aires, Argentina.

出版信息

Int J Pancreatol. 1996 Feb;19(1):61-9. doi: 10.1007/BF02788377.

Abstract

CONCLUSION

Production of excited oxygen species is earlier in the liver than in the pancreas and could contribute to damage in a reflux model. Treatment with SOD could attenuate 59% light emission in pancreas, but did not modify serum enzyme levels or pancreatic edema, resulting as an insufficient isolated therapy. Unexpectedly, it was found an increased plasma antioxidant capacity that was related to total bilirubin levels, and declined at late stages probably denoting other circulating antioxidant consumption.

BACKGROUND

Oxidative stress has been shown to play a role in different models of acute pancreatitis, although it has not been studied in the severe necrohemorrhagic model produced by closed duodenal loop pancreatitis.

METHODS

We studied Sprague Dawley female rats in two groups: a closed duodenal loop pancreatitis group and a control, sham-operated group. In order to evidence the oxygen excited species production, in situ spontaneous chemiluminescence from living and naturally perfused pancreas and liver was measured at 0, 0.5, 1.5, 3, 6, 12, and 24 h after the duodenal ligature. Blood pancreatic amylase and aminotransferases levels were determined as expression of tissue damage in pancreas and liver. At the same time, plasma antioxidant capacity was measured by the peroxyl radical trapping capability of plasma samples compared to that of Trolox (synthetic analog of vitamin E), and results are expressed as Trolox equivalence. Bovine superoxide dismutase (SOD) was administered to attenuate oxygen free radicals activity at the beginning of the peroxidation chain and also as a therapeutic tool.

RESULTS

The experimental procedure induced a severe pancreatitis, as evidenced by pancreatic enzymes that rose markedly in the early hours of disease and remained heightened throughout the experiment. The results show early light emission from the liver at 3 h and peak levels at 12 h, whereas in the pancreas, luminescence increased at 6 h and doubled later at 12 h, both returning to control levels at 24 h.

摘要

结论

肝脏中活性氧的产生早于胰腺,在反流模型中可能导致组织损伤。超氧化物歧化酶(SOD)治疗可使胰腺光发射减弱59%,但未改变血清酶水平或胰腺水肿情况,说明单一使用SOD治疗效果欠佳。意外的是,血浆抗氧化能力增加,且与总胆红素水平相关,在疾病后期下降,这可能意味着其他循环抗氧化剂的消耗。

背景

氧化应激在不同的急性胰腺炎模型中发挥作用,然而,在闭合十二指肠襻性胰腺炎导致的严重坏死性出血模型中尚未进行研究。

方法

我们将雌性斯普拉格-道利大鼠分为两组:闭合十二指肠襻性胰腺炎组和假手术对照组。为了证实活性氧的产生,在十二指肠结扎后0、0.5、1.5、3、6、12和24小时,测量自然灌注状态下的胰腺和肝脏原位自发化学发光。测定血中胰腺淀粉酶和转氨酶水平,作为胰腺和肝脏组织损伤的指标。同时,通过将血浆样本与维生素E的合成类似物Trolox相比,测定血浆样本的过氧自由基捕获能力,来衡量血浆抗氧化能力,并以Trolox当量表示结果。在过氧化反应开始时给予牛超氧化物歧化酶(SOD)以减弱自由基活性,并作为一种治疗手段。

结果

实验过程引发了严重的胰腺炎,疾病早期胰腺酶显著升高并在整个实验过程中持续上升。结果显示,肝脏在3小时开始出现早期光发射,并在12小时达到峰值水平;而胰腺在6小时发光增强,并在12小时加倍,两者在24小时均恢复到对照水平。

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