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

Autor:	Cho K; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea., Lee HG; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea., Piao JY; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea., Kim SJ; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea., Na HK; Department of Food Science and Biotechnology, College of Knowledge-based Services Engineering, Sungshin Women's University, Seoul, Korea., Surh YJ; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea.; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Korea.; Cancer Research Institute, Seoul National University, Seoul, Korea.
Jazyk:	angličtina
Zdroj:	Journal of cancer prevention [J Cancer Prev] 2021 Jun 30; Vol. 26 (2), pp. 118-127.
DOI:	10.15430/JCP.2021.26.2.118
Abstrakt:	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. Competing Interests: CONFLICTS OF INTEREST No potential conflicts of interest were disclosed. (Copyright © 2021 Korean Society of Cancer Prevention.)
Databáze:	MEDLINE
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