Peroxiredoxin I protects gastric mucosa from oxidative injury induced by H-pylori infection
Peroxiredoxin I protects gastric mucosa from oxidative injury induced by H-pylori infection
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DOI：
10.1111/j.1440-1746.2007.05217.x
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发表时间：
2008-04-01
影响因子：
4.1
通讯作者：
Hyodo, Ichinosuke
中科院分区：
文献类型：
--
作者：
Sato, Daisuke;Yanaka, Akinori;Hyodo, Ichinosuke
背景与目的：幽门螺杆菌（Helicobacter pylori，H.幽门螺杆菌）感染增强了活性氧和过氧亚硝酸盐的产生，从而导致氧化性组织损伤。在这项研究中，我们研究了过氧化物酶I（Prx I），一种应激诱导的抗氧化酶，在保护胃粘膜免受H。方法：将野生型（Prx I+/+）和Prx I缺陷型（Prx I-/-）小鼠在感染或不感染幽门螺杆菌的情况下饲养2 ~ 12个月。pylori，悉尼株-1。通过免疫印迹分析和免疫组化评估胃粘膜Prx I的表达。胃炎的程度通过更新的悉尼系统和粘膜炎性细胞因子（MIP-2、IL-1 β和TNF-α）水平进行评价。分别用8-羟基-2 ′-脱氧鸟苷和单链DNA抗体染色法检测黏膜DNA氧化损伤和细胞凋亡。pylori感染可上调Prx I+/+小鼠胃粘膜Prx I的表达，但对Prx I-/-小鼠无影响。H. pylori感染还导致Prx I-/-小鼠比Prx I+/+小鼠更严重的胃炎和更显著的MIP水平升高、更显著的DNA氧化损伤和更显著的细胞凋亡。在没有H。pylori感染后，Prx I+/+和Prx I-/-小鼠胃粘膜无明显变化。pylori感染可上调胃粘膜Prx I的表达，Prx I在胃粘膜抗H.幽门感染
Background an Aim: Helicobacter pylori (H. pylori) infection enhances the production of reactive oxygen species and peroxynitrite, thereby resulting in oxidative tissue damage. In this study, we examined the role of peroxiredoxin I (Prx I), a stress-induced antioxidant enzyme, in protecting gastric mucosa from H. pylori-induced gastric mucosal injury.Methods: Wild type (Prx I+/+) and Prx I-deficient type (Prx I-/-) mice were maintained for 2 to 12 months with or without infection of H. pylori, Sydney strain-1. Gastric mucosal expression of Prx I was assessed by immunoblot analysis and immunohistochemistry. The degree of gastritis was evaluated by the updated Sydney system and by mucosal levels of inflammatory cytokines (MIP-2, IL-1 beta, and TNF-alpha). Oxidative DNA injury and apoptosis were analyzed by mucosal level of 8-hydroxy-2'-deoxyguanosine, and the number of apoptotic cells stained with a single-stranded DNA antibody, respectively.Results: H. pylori infection upregulated gastric mucosal Prx I expression in the Prx I+/+ but not the Prx I-/- mice. H. pylori infection also induced more severe gastritis and a more prominent increase in MIP level, more marked oxidative DNA injury, and apoptosis in the Prx I-/- than the Prx I+/+ mice. In the absence of H. pylori infection, no changes were demonstrated in gastric mucosa in either the Prx I+/+ or the Prx I-/- mice.Conclusion: These data suggest that H. pylori infection upregulates gastric mucosal Prx I expression, and further, that Prx I plays an important role in gastric mucosal protection against oxidative injury induced by H. pylori infection.