N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Helicobacter pylori Infection.
N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Helicobacter pylori Infection.
复制标题
N-乙酰半胱氨酸减少幽门螺杆菌感染诱导的 ROS 介导的氧化性 DNA 损伤和 PI3K/Akt 通路激活
DOI：
10.1155/2018/1874985
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发表时间：
2018
影响因子：
--
通讯作者：
Shu X
中科院分区：
文献类型：
--
作者：
Xie C;Yi J;Lu J;Nie M;Huang M;Rong J;Zhu Z;Chen J;Zhou X;Li B;Chen H;Lu N;Shu X
H.幽门螺杆菌感染可诱导胃上皮细胞活性氧（ROS）相关的DNA损伤并激活PI 3 K/Akt通路。N-乙酰半胱氨酸（NAC）是一种活性氧的抑制剂;幽门相关疾病尚不清楚。 本研究旨在探讨活性氧在H.幽门相关疾病 建立了体外共培养体系和体内Balb/c小鼠H.建立幽门感染的胃上皮细胞。H.采用彗星试验和荧光二氯荧光素试验检测pylori感染对DNA损伤和ROS的影响。Western blotting检测PI 3 K/Akt通路相关蛋白的表达水平。用离体和体内H. pylori感染模型。 结果表明，在体外和体内，H. pylori感染可引起胃上皮细胞ROS水平升高和DNA损伤。NAC处理可有效降低GES-1细胞和Balb/c小鼠胃粘膜的ROS水平，抑制DNA损伤。H. pylori感染诱导ROS介导的PI 3 K/Akt通路激活，NAC治疗抑制了这种作用。然而，NAC治疗组的胃粘膜病理评分与未治疗组相比无显著差异。此外，慢性H. pylori感染降低了Balb/c小鼠胃黏膜APE-1的表达。 ROS水平升高是H. pylori的发病机制，NAC可能对H.幽门相关性胃病与氧化性DNA损伤有关
H. pylori infection induces reactive oxygen species- (ROS-) related DNA damage and activates the PI3K/Akt pathway in gastric epithelial cells. N-Acetylcysteine (NAC) is known as an inhibitor of ROS; the role of NAC in H. pylori-related diseases is unclear. The aim of this study was to evaluate the role of ROS and the protective role of NAC in the pathogenesis of H. pylori-related diseases. An in vitro coculture system and an in vivo Balb/c mouse model of H. pylori-infected gastric epithelial cells were established. The effects of H. pylori infection on DNA damage and ROS were assessed by the comet assay and fluorescent dichlorofluorescein assay. The level of PI3K/Akt pathway-related proteins was evaluated by Western blotting. The protective role of N-acetylcysteine (NAC) was also evaluated with in vitro and in vivo H. pylori infection models. The results revealed that, in vitro and in vivo, H. pylori infection increased the ROS level and induced DNA damage in gastric epithelial cells. NAC treatment effectively reduced the ROS level and inhibited DNA damage in GES-1 cells and the gastric mucosa of Balb/c mice. H. pylori infection induced ROS-mediated PI3K/Akt pathway activation, and NAC treatment inhibited this effect. However, the gastric mucosa pathological score of the NAC-treated group was not significantly different from that of the untreated group. Furthermore, chronic H. pylori infection decreased APE-1 expression in the gastric mucosa of Balb/c mice. An increased ROS level is a critical mechanism in H. pylori pathogenesis, and NAC may be beneficial for the treatment of H. pylori-related gastric diseases linked to oxidative DNA damage.
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影响因子：
1.9
作者：
Papa, A;Danese, S;Gasbarrini, A
通讯作者：
Gasbarrini, A
DOI：
10.1016/j.biocel.2010.04.015
发表时间：
2010-09-01
影响因子：
4
作者：
Cha, Boram;Lim, Joo Weon;Kim, Hyeyong
通讯作者：
Kim, Hyeyong
影响因子：
4.8
作者：
Sokolova, Olga;Bozko, Przemyslaw M.;Naumann, Michael
通讯作者：
Naumann, Michael
胃腺癌中蛋白激酶 B 磷酸化与血管内皮生长因子 A 和微血管密度相关
影响因子：
1.6
作者：
Zhou, X. D.;Chen, H. X.;Lv, N. H.
通讯作者：
Lv, N. H.
影响因子：
2.9
作者：
Xie C;Xu LY;Yang Z;Cao XM;Li W;Lu NH
通讯作者：
Lu NH