胃粘膜细胞增殖在ethanol-induced慢性粘膜损伤与氧化应激和脂质过氧化的老鼠。
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Hernandez-Munoz R, Montiel-Ruiz C, Vazquez-Martinez O
胃粘膜细胞增殖在ethanol-induced慢性粘膜损伤与氧化应激和脂质过氧化的老鼠。
实验室投资。2000年8月,80 (8):1161 - 9。
- PubMed ID
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10950107 (在PubMed]
- 文摘
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氧自由radicals-induced脂质过氧化(LP)与急性ethanol-induced胃粘膜病变的发病机理。然而,LP的角色在慢性胃粘膜损伤的一代是未知的。我们已经开发了一个模型慢性粘膜损伤引起的连续乙醇摄入了5天,以从胃粘膜显著改变等离子体膜。因此,LP是评估在这个实验模型。过氧化活动的指标,粘膜谷胱甘肽含量、胸苷激酶活动(细胞增殖指数)和组胺H2-receptor (H2R)绑定常量量化在动物身上进行胃粘膜损伤。法莫替丁的影响,一个H2R的对手很容易改善慢性粘膜损伤,也是考验。增加自由基在胃炎和LP水平检测;然而,第二,更高的峰值LP在粘膜指出等离子体膜后乙醇提取(恢复期)。这进一步增加了LP恰逢活跃的细胞增殖,减少粘膜谷胱甘肽水平,并减少特定H2R甲氰咪胍绑定。法莫替丁管理加速了粘膜增殖过程,诱导第二lipoperoxidative集早,和保存谷胱甘肽的内容。 In addition, LP correlated directly with cell proliferation and inversely with mucosal membrane cimetidine binding. In conclusion, LP seems to be involved in chronic ethanol-induced gastric mucosal injury. However, a further enhancement of plasma membrane LP occurred, associated with increased DNA synthesis and diminished cimetidine binding by membrane H2R. Therefore, increased LP could also participate in the compensatory mucosal proliferation initiated after ethanol withdrawal.