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首页> 外文期刊>Life sciences >Effect of ellagic acid on gastric damage induced in ischemic rat stomachs following ammonia or reperfusion.
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Effect of ellagic acid on gastric damage induced in ischemic rat stomachs following ammonia or reperfusion.

机译：鞣花酸对氨或再灌注后缺血大鼠胃诱导的胃损害的影响。

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We examined the effect of ellagic acid (EA), one of the polyphenols that are abundantly contained in whisky as a nonalcoholic component, on gastric lesions induced by ammonia plus ischemia or ischemia/reperfusion in rats, in relation to the antioxidative system. Under urethane anesthesia, a rat stomach was mounted in an ex vivo chamber, and the following two experiments were performed; 1) a stomach was made ischemic (1.5 ml/100 g body weight) for 20 min, followed by reperfusion for 15 min in the presence of 100 mM HCl; 2) a stomach was made ischemic by bleeding from the carotid artery (1 ml/100 g body weight), followed by intragastric application of ammonia (NH4OH: 120 mM). EA (0.1-10 mg/ml) was applied in the chamber 30 min before the onset of ischemia. Gastric potential difference (PD) and mucosal blood flow (GMBF) were measured before, during and after 20 min of ischemia. Ischemia/reperfusion caused a profound drop in GMBF followed by a return, and resulted in hemorrhagic lesions in the stomach in the presence of 100 mM HCI. These lesions were dose-dependently prevented by EA with suppression of lipid peroxidation but no effect on GMBF, and the effect at 6 mg/ml was almost equivalent to that of superoxide dismutase (SOD: 15000 unit/kg/hr) infused i.v. during a test-period. On the other hand, application of NH4OH to the ischemic stomach produced a marked reduction in PD, resulting in severe hemorrhagic lesions. These changes were prevented with both EA and SOD. In addition, EA had a potent scavenging action against monochloramine in vitro. These results suggest that EA exhibits gastric protective action against gastric lesions induced by NH4OH or reperfusion in the ischemic stomach, probably due to its anti-oxidative activity. This property of EA partly explains the less damaging effect of whisky in the stomach and may be useful as the prophylactic for Helicobacter pylori-associated gastritis.
机译：我们检查了鞣花酸（EA）（一种作为非酒精性成分的威士忌中大量含有的多酚之一）对由氨加缺血或缺血/再灌注引起的大鼠胃部抗氧化系统的影响。在氨基甲酸乙酯麻醉下，将大鼠胃安装在离体室中，并进行以下两个实验。 1）使胃缺血（1.5 ml / 100 g体重）20分钟，然后在100 mM HCl存在下再灌注15分钟; 2）通过从颈动脉（1ml / 100g体重）出血，然后在胃内施用氨水（NH 4 OH：120mM）使胃局部缺血。在局部缺血发作前30分钟在室中施用EA（0.1-10mg / ml）。在缺血20分钟之前，期间和之后测量胃电位差（PD）和粘膜血流量（GMBF）。缺血/再灌注导致GMBF大幅下降，随后又回升，并在存在100 mM HCl的情况下导致胃部出血性病变。 EA可以剂量依赖性地预防这些病变，同时抑制脂质过氧化，但对GMBF无影响，并且6 mg / ml的作用几乎等同于静脉内输注的超氧化物歧化酶（SOD：15000单位/ kg / hr）。在测试期间。另一方面，将NH4OH施加于缺血性胃部可显着降低PD，从而导致严重的出血性病变。 EA和SOD均阻止了这些更改。此外，EA在体外对一氯胺具有有效的清除作用。这些结果表明，EA可能对由NH4OH引起的胃部病变或缺血性胃的再灌注具有胃保护作用，这可能是由于其抗氧化活性所致。 EA的这种特性部分地解释了威士忌对胃的损害较小，并且可以用作幽门螺杆菌相关胃炎的预防剂。

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