ORIGINAL RESEARCH ARTICLE

Suppression of Helicobacter pylori-induced gastric carcinogenesis by emodin in GES-1 cells through the PI3K/AKT and NRF2 signaling pathways

Palanimuthu Duraisamy1 Karthik Mohan2 Rajasekar Muthusamy3*
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1 Department of Biotechnology, Faculty of Science, Bharathidasan University, Thirucharapalli, Tamil Nadu, India
2 Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamil Nadu, India
3 Central Research Laboratory, Vinayaka Mission’s Kirupananda Variyar Medical College and Hospitals, Vinayaka Mission’s Research Foundation Deemed To Be University, Salem, Tamil Nadu, India
CP 2023, 5(3), 2582
Submitted: 5 May 2023 | Accepted: 30 June 2023 | Published: 16 July 2023
© 2023 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Helicobacter pylori is recognized as a microbial carcinogen among Gram-negative bacteria and is considered the most significant risk factor for the development of human gastric cancer (GS). Consequently, inhibiting the growth of H. pylori has become a critical strategy for preventing GS. This study focuses on the inhibitory effects of emodin (EMN) against H. pylori-induced gastric carcinogenic signaling in human gastric epithelial cells (GES-1). In vitro cytotoxicity assessments revealed that a concentration of 40 μM of EMN provided remarkable protection to gastric cells, resulting in 85% cell viability without inducing toxicity. Furthermore, EMN prevented the H. pylori-induced depletion of antioxidants, which was mediated by reactive oxygen species generation, DNA damage, and nuclear fragmentation. Our findings indicate that EMN significantly suppresses the expression of phosphorylated forms of phosphatidylinositol 3-kinase (PI3K)/AKT, phosphorylated p38 kinases (p-p38), phosphorylated extracellular signal-regulated kinase-1 (p-ERK1), phosphorylated c-Jun N-terminal kinase (p-JNK) in GES-1 cells infected with H. pylori. In addition, EMN notably enhances the expression of antioxidant proteins nuclear factor erythroid factor-2 (NRF2) in H. pylori-infected cells. In summary, EMN demonstrates promising potential in preventing H. pylori-associated infections and the subsequent development of resistance, making it a viable candidate for the prevention of H. pylori-induced GS.

Keywords
Emodin
Gastric cancer
Helicobacter pylori
GES-1 cell line
Inflammation
Funding
None.
Conflict of interest
The authors declare that they have no competing interests.
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