Document Type : Original Article
Authors
1
Medical Physiology departement, Faculty of Medicine, Tanta University, Tanta, Egypt
2
Pharmacology Department, Faculty of Medicine, Tanta University, Tanta, Egypt.
3
Medical Biochemistry Department, Faculty of Medicine, Tanta University, Tanta, Egypt.
4
Anatomy and Embryology Department, Faculty of Medicine, Tanta University, Tanta, Egypt.
Abstract
Background: Gastric ulcer is one of the most ubiquitous gastrointestinal tract disorders, causing high morbidity. The goal of this study was to explore at the mechanistic effects of Baicalein (BA) and/or Empagliflozin (EMP) treatment on gastric ulcer caused by indomethacin and prednisolone, with an emphasis on the role of the HO-1/SIRT1 / HMGB1 signaling pathway.
Material and methods: Fifty adult albino rats were allocated into 5 equal groups: control, ulcer (Prednisolone 10mg/kg for 6 days followed by indomethacin as single oral dose 30 mg/kg), BA (30 mg/kg), EMP (10 mg/kg), and BA + EMP groups. The volume of gastric juice, pH, free and total acidity was estimated. The gene expression of HO-1 and SIRT1 in gastric tissues was assessed by qRT -PCR. Biochemical analysis of gastric tissues homogenates including HMGB-1, PGE2 & nitrites levels was performed. Assay of inflammatory markers and redox status were detected. Additionally, histological, scanning electron microscopic and immunohistochemical analyses were determined.
Results: After 4 weeks of treatment, there was remarkable improvement of the histological architecture of rat gastric tissues. Upregulation of HO-1 and SIRT1 gene expression, as well as a decrease in HMGB1 level, resulted in improved inflammatory and oxidative stress biomarkers. Furthermore, immunohistochemical analysis revealed increase in Bcl-2 expression and decreased expression of Bax in the treated groups.
Conclusion: Concurrent usage of BA & EMP against gastric ulcer in rats could be related to the interaction of their anti-oxidant, anti-inflammatory, and anti-apoptotic activities via modulation of HO-1/SIRT1 / HMGB1 signaling pathway.
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