Abstract
Multiple theories have been proposed describing the pathogenic mechanisms of
(
)-associated gastric motility disorders. We assessed ex vivo pyloric activity in
-infected rats, and tried to explore the associated ghrelin hormone alteration and pyloric fibrogenesis. In addition, miR-1 was assessed in pyloric tissue samples, being recently accused of having a role in smooth muscle dysfunction. Ninety adult male Wistar albino rats were assigned into nine groups:
) control group,
) sterile broth (vehicle group),
) amoxicillin control,
) omeperazole control,
) clarithromycin control,
) triple therapy control,
)
- group,
)
-clarithromycin group, and
)
-triple therapy group. Urease enzyme activity was applied as an indicator of
infection. Ex vivo pyloric contractility was evaluated. Serum ghrelin was assessed, and histological tissue evaluation was performed. Besides, pyloric muscle miR-1 expression was measured. The immunological epithelial to mesenchymal transition (EMT) markers; transforming growth factor β (TGFβ), α-smooth muscle actin (α-SMA), and E-cadherin-3 were also evaluated. By
infection, a significant (
< 0.001) reduced pyloric contractility index was recorded. The miR-1 expression was decreased (
< 0.001) in the
infected group, associated with reduced serum ghrelin, elevated TGFβ, and α-SMA levels and reduced E-cadherin levels. Decreased miR-1 and disturbed molecular pattern were improved by treatment. In conclusion,
infection was associated with reduced miR-1, epithelial to mesenchymal transition, and pyloric hypomotility. The miR-1 may be a target for further studies to assess its possible involvement in
-associated pyloric dysfunction, which might help in the management of human
manifestations and complications.
This work is investigating functional, histopathological, and molecular changes underlying
hypomotility and is correlating these with miR-1, whose disturbance is supposed to be involved in smooth muscle dysfunction and cell proliferation according to literature. Epithelial to mesenchymal transition and reduced ghrelin hormone may contribute to
infection-associated hypomotility.
infection was associated with reduced pyloric miR-1 expression. Targeting miR-1 could be valuable in the clinical management of pyloric hypofunction.