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食管-胃-十二指肠黏膜对酸和胆汁产生的自由基

Free radical production in the esophago-gastro-duodenal mucosa in response to acid and bile.

作者信息

Boni L, Benevento A, Shimi S M, Cuschieri A

机构信息

Department of Surgical Science, University of Insubria, Varese-Italy.

出版信息

Dis Esophagus. 2006;19(2):99-104. doi: 10.1111/j.1442-2050.2006.00548.x.

Abstract

Several studies have demonstrated the role of free radicals in causing esophagus-gastro-duodenal mucosal injury. The present study has been designed to investigate: whether acid, bile salts and a combination of bile + acid could determine the production of O2-derived free radicals by oesophageal, gastric and duodenal mucosa; which agent is capable of producing more free radicals and if O2-derived free radicals production depends on the duration of contact with acid, bile salts and their combination. Wistar rats' gastro-intestinal mucosa were perfused with bile, acid and a combination of bile + acid at pH4 and pH2 for 1 hour and 2 hours. Free radical production (FRP) was assessed by chemoluminescence. After 1 hour, the increase in FRP in comparison with control reached statistical significance (P < 0.05) at all tested pH levels in the duodenum, at pH1, 2 and 3 in the esophagus, and at pH1 in the stomach. Comparing different segments, both the esophagus and duodenum behaved similarly, producing more free radicals than the stomach at all pH values. However, this difference reached statistical significance at pH1 and 2 only. In comparison to control, FRP was increased by bile (pH7) infusion after 1 and 2 hours. There was increased FRP in all segments after the infusion of bile at pH2 and 4 in comparison to control. Infusion of bile at pH2 stimulates more FRP than infusion of bile at pH4 in all segments. This increased FRP reaches statistical significance in the esophagus after 2 hours of infusion, in the stomach after 1 and 2 hours of infusion, but in the duodenum it does not reach statistical significance. Acid, bile and bile + acid at pH2 and 4 can cause free radical production in esophageal, gastric and duodenal mucosa. Their role in producing free radicals is different according to the segment and the chemical composition of the solution.

摘要

多项研究已证实自由基在导致食管 - 胃 - 十二指肠黏膜损伤中所起的作用。本研究旨在调查:酸、胆盐以及胆盐 + 酸的组合是否会促使食管、胃和十二指肠黏膜产生源自O₂的自由基;哪种试剂能够产生更多自由基,以及源自O₂的自由基产生是否取决于与酸、胆盐及其组合的接触时长。将Wistar大鼠的胃肠道黏膜在pH4和pH2条件下分别用胆汁、酸以及胆盐 + 酸的组合灌注1小时和2小时。通过化学发光法评估自由基产生量(FRP)。1小时后,与对照组相比,十二指肠在所有测试pH水平下、食管在pH1、2和3时以及胃在pH1时,FRP的增加均达到统计学显著性(P < 0.05)。比较不同节段,食管和十二指肠表现相似,在所有pH值下产生的自由基均多于胃。然而,这种差异仅在pH1和2时达到统计学显著性。与对照组相比,灌注胆汁(pH7)1小时和2小时后FRP增加。与对照组相比,在pH2和4灌注胆汁后所有节段的FRP均增加。在所有节段中,pH2灌注胆汁比pH4灌注胆汁刺激产生更多的FRP。这种增加的FRP在食管灌注2小时后、胃灌注1小时和2小时后达到统计学显著性,但在十二指肠未达到统计学显著性。pH2和4的酸、胆汁以及胆盐 + 酸可导致食管、胃和十二指肠黏膜产生自由基。它们在产生自由基方面的作用因节段和溶液的化学成分而异。

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