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Journal of Cancer Prevention

Original Article

J Cancer Prev 2021; 26(2): 118-127

Published online June 30, 2021

© Korean Society of Cancer Prevention

Protective Effects of Silibinin on Helicobacter pylori-induced Gastritis: NF-κB and STAT3 as Potential Targets

Kyunghwa Cho1 , Hee Geum Lee1 , Juan-Yu Piao1 , Su-Jung Kim1 , Hye-Kyung Na2 , Young-Joon Surh1,3,4

1Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, 2Department of Food Science and Biotechnology, College of Knowledge-based Services Engineering, Sungshin Women's University, 3Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, 4Cancer Research Institute, Seoul National University, Seoul, Korea

Correspondence to :
Young-Joon Surh, E-mail:,

Received: January 6, 2021; Revised: February 24, 2021; Accepted: February 24, 2021

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


More than half of the world’s populations are considered to be infected by Helicobacter pylori. It causes a chronic inflammation of the stomach, which is implicated in the pathogenesis of gastric ulcer and cancer. Silibinin, a polyphenolic flavonoid derived from milk thistle, has been known for its hepatoprotective effects, and recent studies have revealed its chemopreventive potential. In the present study, we examined the anti-inflammatory effects of silibinin in human gastric cancer MKN-1 cells and in the stomach of C57BL/6 mice infected by H. pylori. Pretreatment with silibinin attenuated the up-regulation of COX-2 and inducible nitric oxide synthase (iNOS) in H. pylori-infected MKN-1 cells and mouse stomach. In addition, the elevated translocation and DNA binding of NF- κB and STAT3 induced by H. pylori infection were inhibited by silibinin treatment. Moreover, H. pylori infection in combination with high salt diet resulted in dysplasia and hyperplasia in mouse stomach, and these pathological manifestations were substantially mitigated by silibinin administration. Taken together, these findings suggest that silibinin exerts anti-inflammatory effects against H. pylori infection through suppression of NF-κB and STAT3 and subsequently, expression of COX-2 and iNOS.

Keywords: Helicobacter pylori, Silibinin, NF-κB, STAT3, Gastritis

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