A polysaccharide from Aloe vera L. var. chinensis (Haw.) Berger prevents damage to human gastric epithelial cells in vitro and to rat gastric mucosa in vivo

2016 ◽  
Vol 24 ◽  
pp. 501-512 ◽  
Author(s):  
Chen Xu ◽  
Chen Ding ◽  
Nan Zhou ◽  
Xiao-Ming Ruan ◽  
Bin-Xin Guo
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Aloe Vera ◽  
Gastric Epithelial Cells ◽  
Rat Gastric Mucosa

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

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Chuan Xie ◽  
Jian Yi ◽  
Jing Lu ◽  
Muwen Nie ◽  
Meifang Huang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Oxidative Dna Damage ◽  
Akt Pathway ◽  
Gastric Epithelial Cells ◽  
H Pylori

Background. 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. Aim. 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. Method. 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. Results. 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. Conclusions. 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.

Actions of prostacyclin (PGI2) and its product, 6-oxo-PGF1α on the rat gastric mucosa in vivo and in vitro

1978 ◽  
Vol 15 (6) ◽  
pp. 955-967 ◽  
Author(s):  
B.J.R. Whittle ◽  
N.K. Boughton-Smith ◽  
S. Moncada ◽  
J.R. Vane
Keyword(s):  
Gastric Mucosa ◽  
Rat Gastric Mucosa

scholarly journals Effect of Glucocorticoid on Expression of Rat MUC5AC mRNA in Rat Gastric Mucosa in Vivo and in Vitro.

2001 ◽  
Vol 24 (6) ◽  
pp. 634-637 ◽  
Author(s):  
Toru TANAKA ◽  
Taketo KOBAYASHI ◽  
Kastuyoshi SUNAGA ◽  
Satoru TANI
Keyword(s):  
Gastric Mucosa ◽  
Rat Gastric Mucosa

scholarly journals Regulation of Human β-Defensins by Gastric Epithelial Cells in Response to Infection with Helicobacter pylori or Stimulation with Interleukin-1

2000 ◽  
Vol 68 (9) ◽  
pp. 5412-5415 ◽  
Author(s):  
Deborah A. O'Neil ◽  
Sheri P. Cole ◽  
Edith Martin-Porter ◽  
Michael P. Housley ◽  
Lide Liu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Interleukin 1 ◽  
Peptide Antibiotic ◽  
Gastric Epithelial Cells ◽  
Proinflammatory Mediators ◽  
H Pylori

ABSTRACT Gastric epithelial cells in vitro and in vivo are shown to constitutively express the peptide antibiotic human β-defensin type 1 (hBD-1). In contrast, hBD-2 expression is regulated in gastric epithelial cells and increases in response to infection withHelicobacter pylori or stimulation with the proinflammatory cytokine interleukin-1. These data suggest that hBD-2 is a component of the regulated host gastric epithelial cell response to H. pylori infection and proinflammatory mediators.

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