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首页> 外文期刊>World Journal of Gastroenterology >A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48/80 in rats.
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A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48/80 in rats.

机译：胃粘膜抗坏血酸在化合物48/80诱导的大鼠急性胃粘膜损伤进展中的关键作用。

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AIM: To study the role of gastric mucosal ascorbic acid (AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats. METHODS: C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80 treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitriteitrate (NOx), non-protein SH (NPSH), and myeloperoxidase (MPO), and serum total AA, reduced AA, oxidized AA, and NOx were conducted 0.5 and 3 h after C48/80 treatment. RESULTS: Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment. Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment, but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h. Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently. CONCLUSION: Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.
机译：目的：研究肥大细胞脱粒剂化合物48/80（C48 / 80）诱导的大鼠胃粘膜抗坏血酸（AA）在急性胃粘膜病变中的作用。方法：腹腔注射Wistar大鼠腹腔注射C48 / 80（0.75 mg / kg）。在C48 / 80处理后0.5小时口服AA（10、50或100 mg / kg）。胃黏膜病变严重程度和血流量的测定以及胃黏膜总AA，还原AA，氧化AA，维生素E，硫代巴比妥酸反应性物质（TBARS），粘液黏附，亚硝酸盐/硝酸盐（NOx），非蛋白SH（在C48 / 80处理后0.5和3小时进行了NPSH）和髓过氧化物酶（MPO）以及血清总AA，还原AA，氧化AA和NOx。结果：胃黏膜病变发生在C48 / 80治疗后0.5小时，并在3小时后发展。 C48 / 80治疗后0.5小时胃粘膜血流量减少，但3小时后恢复。 C48 / 80治疗后3小时，胃粘膜总AA，降低的AA，维生素E和粘液黏液浓度降低。 C48 / 80处理后胃粘膜氧化的AA浓度保持不变。 C48 / 80处理后，胃粘膜NPSH浓度降低了0.5小时，但3小时后恢复。 C48 / 80处理后胃粘膜TBARS浓度和MPO活性增加0.5 h，并在3 h进一步增加。 C48 / 80处理后，血清总AA和降低的AA浓度在0.5 h时增加，并在3 h时进一步增加，而血清氧化的AA浓度在0.5 h时增加。 C48 / 80处理后3小时，血清和胃粘膜NOx浓度增加。在治疗后0.5小时，对C48 / 80处理的大鼠施用AA可以防止胃粘膜病变进展和胃粘膜总AA的变化，减少AA，维生素E，黏液，NOx和TBARS的浓度以及MPO活性和血清NOx在治疗后3小时发现的浓度呈剂量依赖性。给予C48 / 80治疗的大鼠AA的剂量依赖性地导致在治疗后3小时血清总AA的进一步增加和AA浓度的降低。结论：胃黏膜AA在C48 / 80诱导的大鼠急性胃黏膜病变过程中起关键作用。

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