Abstract
Helicobacter pylori (H. pylori), a microbial carcinogen of Gram-negative bacteria, has been recognized to be the highest risk factor for the growthof human gastric cancer (GC). Therefore, the inhibition of thegrowth rate of H. pylori has been consideredan effective vital strategy to prevent GC development. This study highlights the inhibitory effect of vicenin-2 against H. pylori-induced gastric carcinogen signaling in human gastric epithelial cells (GES-1). In vitro cytotoxicity studies reported that 40 µM of vicenin-2 remarkably protects the gastric cells and this concentration shows 85% cell viability also does not produce toxicity. In addition, vicenin-2 prevents H. pylori-infected increased depletion of antioxidants mediated by reactive oxygen species generation, DNA damage, malondialdehyde, and nuclear fragmentation. Here, we noticed that vicenin-2 remarkably suppressed the expression range of the phosphorylated form of phosphatidylinositol 3-kinase/protein kinase B, phosphorylated p38 kinases, phosphorylated extracellular signal-regulated kinase-1, phosphorylated c-Jun N-terminal kinase, tumor necrosis factor-α, interleukin-6, cyclooxygenase-2in GES-1 infected with H. pylori. Moreover, we observed that vicenin-2 enhanced the antioxidants protein nuclear factor erythroid factor-2and phosphatase and tensin homologexpression in H. pylori-infected cells. Thus, vicenin-2 prevents the H. pylori-associated infection, and its resistance might be a potential strategyin preventing GC induced by H. pylori.
Published Version
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