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Original Research Article | OPEN ACCESS

Effect of omeprazole on gastric mucosal damage and PI3K-Akt signaling pathway in infant mice infected with Helicobacter pylori

Xiaoyan Fan, Si Zhang1, Dan Yin1, Ali Pang2

1Department of Pediatric Gastroenterology, Jiujiang Maternal and Child Health Hospital, Jiujiang 332000, Jiangxi Province, China; 2Department of Student Management, Jiujiang University, Jiujiang 332000, Jiangxi Province, China.

For correspondence:-  Ali Pang   Email: m1303p@163.com

Accepted: 29 November 2021        Published: 30 December 2021

Citation: Fan X, Zhang S, Yin D, Pang A. Effect of omeprazole on gastric mucosal damage and PI3K-Akt signaling pathway in infant mice infected with Helicobacter pylori. Trop J Pharm Res 2021; 20(12):2527-2532 doi: 10.4314/tjpr.v20i12.10

© 2021 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 determine the impact of omeprazole on gastric mucosa injury in young mice with Helicobacter pylori (Hp) infection, and underlying mechanism.
Methods: The young mice were assigned to control, model and drug groups. The control group was not treated, while model and drug groups were mice with Hp infection. Mice in the model group were given omeprazole. The mRNA and protein expression levels of PIEN, PI3K, AKT and P-Akt were assayed with real-time PCR and Western blotting, respectively.
Results: The mRNA levels of PI3K, AKT and P-Akt were significantly increased in model mice, relative to controls, while PIEN mRNA levels were lower (p < 0.05). The mRNA and protein expressions of PI3K, AKT and P-Akt were significantly down-regulated in drug group, relative to model mice (F = 131.750, p < 0.05; F = 268.440, p < 0.05; F = 91.560, p < 0.05).
Conclusion: Omeprazole reduces inflammatory response, improves oxidative stress response, and alleviates gastric mucosal damage in young mice infected with Helicobacter pylori, probably through a mechanism related to the regulation of mRNA and protein expressions in PI3K-Akt signal route. This finding may be useful in the development of new drugs for protection against gastric mucosal lesion.

Keywords: Omeprazole, Helicobacter pylori infection, Gastric mucosal injury, PI3K-Akt signaling pathway

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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