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首页> 美国卫生研究院文献>World Journal of Gastroenterology >Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats
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Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats

机译：马来酸伊索拉定抑制吲哚美辛诱导的大鼠促炎细胞因子升高和胃损伤

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AIM: To investigate the mucosal protective effect and the mechanisms of action of the anti-ulcer drug irsogladine maleate in gastric injury induced by indomethacin in rats.METHODS: Gastric mucosal injury was induced in male Hos:Donryu rats by oral administration of indomethacin at a dose of 48 mg/kg. One hour before indomethacin treatment, animals were orally pretreated with irsogladine maleate at doses of 1 mg/kg, 3 mg/kg or 10 mg/kg. Four hours after indomethacin administration, the animals were sacrificed and their stomachs were rapidly removed and processed for the evaluation of gastric mucosal damage and the determination of the concentrations of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-8 and myeloperoxidase (MPO) in mucosal tissues.RESULTS: Linear hemorrhagic mucosal lesions were observed primarily in the glandular stomach 4 h after oral administration of indomethacin. Pretreatment with irsogladine maleate markedly reduced the number and severity of these lesions in a dose-dependent manner. The mucosal concentrations of proinflammatory cytokines (TNF-α, IL-1β, and IL-8) and MPO, which indicates the degree of mucosal infiltration by neutrophils, increased concomitantly with the occurrence of gastric injury in the indomethacin-treated rats. Pretreatment with irsogladine maleate significantly decreased the levels of these inflammatory factors in gastric tissue elicited by indomethacin.CONCLUSION: The mucosal protective effects afforded by irsogladine maleate on gastric injury induced by indomethacin are mediated by inhibition of mucosal proinflammatory cytokine production and neutrophil infiltration, leading to suppression of mucosal inflammation and subsequent tissue destruction.
机译：目的：探讨吲哚美辛对大鼠胃溃疡的黏膜保护作用及抗溃疡药物马来酸伊索格列汀的作用机制：方法：口服吲哚美辛对雄性Hos：Donryu大鼠胃黏膜损伤。剂量为48 mg / kg。消炎痛治疗前一小时，以1 mg / kg，3 mg / kg或10 mg / kg的剂量口服马来酸伊格列汀预处理动物。吲哚美辛给药后四小时，处死动物并迅速摘除它们的胃并进行处理，以评估胃粘膜损伤并确定肿瘤坏死因子-α（TNF-α），白介素-1β（IL-1β）的浓度。结果：口服吲哚美辛4 h后，主要在腺胃中观察到线性出血性粘膜损害。用马来酸伊索拉定预处理可显着降低这些病变的数量和严重程度，且呈剂量依赖性。随着消炎痛治疗大鼠胃部损伤的发生，促炎性细胞因子（TNF-α，IL-1β和IL-8）和MPO的黏膜浓度随中性粒细胞的黏膜浸润程度而增加。结论：吲哚美辛引起的胃黏膜保护作用是通过抑制黏膜促炎性细胞因子的产生和中性粒细胞浸润而介导的，从而可降低吲哚美辛引起的胃组织炎症因子的含量。结论：抑制粘膜炎症和随后的组织破坏。

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