Preventative Effect of Astaxanthin Against Helicobacter pylori-Induced Proliferation of Gastric Epithelial Cells via the Suppression of Wnt/β-Catenin Signaling Pathway.

OBJECTIVES: Helicobacter pylori (H. pylori) infection has been regarded as a major risk factor for gastric cancer. Various In vivo and in vitro studies have reported that H. pylori infection induces hyper-proliferation, a hallmark of carcinogenesis, in gastric epithelial cells by activating Wnt/β-catenin signaling pathway. Wnt/β-catenin signaling is associated with cell proliferation, which is believed to be linked to various types of human cancer when β-catenin is over-accumulated in the cytoplasm and translocated into the nucleus. Astaxanthin is a reddish carotenoid pigment that has powerful anti-oxidant, anti-inflammatory, and anti-microbial properties. We aim to investigate whether astaxanthin inhibits H. pylori-induced hyper-proliferation in gastric epithelial cells by suppressing Wnt/β-catenin signaling pathway. METHODS: The AGS cell line (a human gastric adenocarcinoma cell-line), H. pylori (NCTC 11,637 strain), and Astaxanthin were used. Cell viability was assessed by WST assay and Colony forming assay. Levels of proteins involved in Wnt/β-catenin signaling pathway were measured by Western blot assay. Real-time PCR assay was used to measure mRNA expression of oncogenes such as c-myc and cyclin E. RESULTS: H. pylori stimulation increased levels of proteins involved in Wnt/β-catenin signaling pathway. mRNA expression of oncogenes such as c-myc and cyclin E were also elevated by H. pylori stimulation. Astaxanthin suppressed cell growth in H. pylori–stimulated AGS cells. Levels of Wnt/β-catenin signaling pathway proteins were decreased by astaxanthin treatment in H. pylori-stimulated AGS cells. CONCLUSIONS: This study suggested that AST may inhibit H. pylori-induced hyper-proliferation by suppressing Wnt/β-catenin signaling pathway. FUNDING SOURCES: BK21 FOUR.