Descripción

Control condition micrograph from the H. pylori infection study, showing baseline gastric epithelial cell morphology without bacterial exposure or N-acetylcysteine treatment.

Figure 1

Micrograph

Source Paper

N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Helicobacter pylori Infection.

Oxidative medicine and cellular longevity (2018)

PMID: 29854076

DOI: 10.1155/2018/1874985

Cite This Figure

![Figure 1: Control condition micrograph from the H. pylori infection study, showing baseline gastric epithelial cell morphology without bacterial exposure or N-acetylcysteine treatment.]()

> Source: Chuan Xie et al. "N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway ." *Oxidative medicine and cellular longevity*, 2018. PMID: [29854076](https://pubmed.ncbi.nlm.nih.gov/29854076/)

<figure>
  <img src="" alt="Control condition micrograph from the H. pylori infection study, showing baseline gastric epithelial cell morphology without bacterial exposure or N-acetylcysteine treatment." />
  <figcaption>Figure 1. Control condition micrograph from the H. pylori infection study, showing baseline gastric epithelial cell morphology without bacterial exposure or N-acetylcysteine treatment.<br>  Source: Chuan Xie et al. "N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway ." <em>Oxidative medicine and cellular longevity</em>, 2018. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/29854076/">29854076</a></figcaption>
</figure>

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