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Original Research Article | OPEN ACCESS

Curculigoside attenuates Helicobacter pylori-induced inflammation and apoptosis of gastric mucosal epithelial cells via NF-κB pathway

Yongjian Li1, Xiaoyan Su2

1Department of Pediatrics, Hangzhou Ninth People's Hospital, Hangzhou, Zhejiang Province 311200, China; 2Department of Pediatrics, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province 310012, China.

For correspondence:-  Xiaoyan Su   Email: suxiaoyan_0616@163.com   Tel:+8657189975912

Accepted: 31 October 2022        Published: 30 November 2022

Citation: Li Y, Su X. Curculigoside attenuates Helicobacter pylori-induced inflammation and apoptosis of gastric mucosal epithelial cells via NF-κB pathway. Trop J Pharm Res 2022; 21(11):2367-2373 doi: 10.4314/tjpr.v21i11.14

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the possible effects and mechanisms of action of curculigoside (Cur) on gastric ulcers.
Methods: Human gastric mucosal epithelial GES-1 cells were infected with Helicobacter pylori and then treated with Cur. Cell counting kit 8 (CCK-8), flow cytometry, and immunofluorescence assays were used to investigate the effect of Cur on cell viability and apoptosis after exposure to H. pylori. Inflammation status and reactive oxygen species (ROS) were assessed using enzyme-linked immunoassay (ELISA) and dichlorodihydrofluorescein (DCF) staining, respectively, while immunoblot and immunofluorescence assays were performed to determine the effect of Cur on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.
Results: Cur significantly increased H. pylori-induced cell viability and inhibited H. pylori-induced inflammatory cytokine production (p < 0.01). Furthermore, Cur significantly suppressed H. pylori-induced ROS production and apoptosis (p < 0.01). Through the NF-κB pathway, Cur attenuated H. pylori-induced inflammation and apoptosis of gastric mucosal epithelial cells.
Conclusion: In H. pylori infection, Cur treatment increases cell viability, reduces inflammatory cytokine production, suppresses ROS production, and inhibits apoptosis via NF-κB pathway. Further investigation using whole animal experiments would be needed to establish the role of Cur in the management of H. pylori-induced gastric ulcers.

Keywords: Gastric ulcers, Curculigoside, Inflammation, Apoptosis, NF-κB pathway

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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