乙酰半胱氨酸降低 感染诱导的 ROS 介导的氧化 DNA 损伤和 PI3K/Akt 通路激活。
-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Infection.
机构信息
Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Department of Gastroenterology, Yichun People's Hospital, Yichun, Jiangxi 336000, China.
出版信息
Oxid Med Cell Longev. 2018 Apr 26;2018:1874985. doi: 10.1155/2018/1874985. eCollection 2018.
BACKGROUND
infection induces reactive oxygen species- (ROS-) related DNA damage and activates the PI3K/Akt pathway in gastric epithelial cells. -Acetylcysteine (NAC) is known as an inhibitor of ROS; the role of NAC in -related diseases is unclear.
AIM
The aim of this study was to evaluate the role of ROS and the protective role of NAC in the pathogenesis of -related diseases.
METHOD
An coculture system and an Balb/c mouse model of -infected gastric epithelial cells were established. The effects of 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 -acetylcysteine (NAC) was also evaluated with and infection models.
RESULTS
The results revealed that, and , 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. 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 infection decreased APE-1 expression in the gastric mucosa of Balb/c mice.
CONCLUSIONS
An increased ROS level is a critical mechanism in pathogenesis, and NAC may be beneficial for the treatment of -related gastric diseases linked to oxidative DNA damage.
背景
感染会在胃上皮细胞中诱导活性氧物质（ROS）相关的 DNA 损伤，并激活 PI3K/Akt 通路。乙酰半胱氨酸（NAC）是一种 ROS 抑制剂；NAC 在相关疾病中的作用尚不清楚。
目的
本研究旨在评估 ROS 在相关疾病发病机制中的作用以及 NAC 的保护作用。
方法
建立了一种共培养系统和一种感染胃上皮细胞的 Balb/c 小鼠模型。通过彗星试验和荧光二氯荧光素试验评估感染对 DNA 损伤和 ROS 的影响。通过 Western blot 评估 PI3K/Akt 通路相关蛋白的水平。还使用感染模型评估了 N-乙酰半胱氨酸（NAC）的保护作用。
结果
结果表明，感染增加了胃上皮细胞中的 ROS 水平并诱导了 DNA 损伤。NAC 处理可有效降低 GES-1 细胞和 Balb/c 小鼠胃黏膜中的 ROS 水平并抑制 DNA 损伤。感染诱导了 ROS 介导的 PI3K/Akt 通路激活，NAC 处理抑制了这种作用。然而，NAC 处理组的胃黏膜病理评分与未处理组无显著差异。此外，慢性感染降低了 Balb/c 小鼠胃黏膜中的 APE-1 表达。
结论
ROS 水平升高是发病机制中的一个关键机制，NAC 可能有益于治疗与氧化 DNA 损伤相关的相关胃部疾病。
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