Iranian
Biomedical Journal
Volume 28, Issue 7 (Special Issue 2024)
IBJ 2024, 28(7): 46-46 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Ataee M M, Rostamani A, Moslehi A. Protective Effects of Rosmarinic Acid on Ethanol-Induced Gastritis in Male Rats. IBJ 2024; 28 (7) :46-46
URL: http://ibj.pasteur.ac.ir/article-1-4422-en.html
URL: http://ibj.pasteur.ac.ir/article-1-4422-en.html
Abstract:
Introduction: Alcohol increases superoxide anion and decreases non-protein sulfhydryl groups such as glutathione (GSH) in the mucosal layer. Superoxide anions then react with membrane lipids and produce lipid peroxides. Malondialdehyde (MDA) is a significant product of lipid peroxidation. Today, the main strategies for improving gastric injuries are proton pump inhibitors, histamine type 2 receptor blockers, and anti-acids. Rosmarinic acid (RA) is a synthetic compound commonly found in plants from the Lamiaceae family, including Rosmarinus officinalis (rosemary). Studies have revealed that RA decreases MDA as a marker of lipid peroxidation in the cell membrane and increases GSH and GSH peroxidase as antioxidant defenses. This study aimed to evaluate the effects of RA on preserving gastric mucosal layer integrity and glands and protecting gastric ulcers in ethanol-induced gastritis.
Methods and Materials: Animals were randomly divided into seven equal groups, six each, including a control group. After one hour of ethanol gavage, the animals received 50 mg/kg of sodium thiopental (intraperitoneal) and were sacrificed. The abdomen was exposed, and the stomach was removed.
Results: RA increased mucosal thickness, decreased gastric ulcers, enhanced the number of mucosal, chief, and parietal cells, decreased the presence of mucosal and submucosal leucocytes, reduced the number of gastric blood vessels in the mucosal and submucosal layers, increased gastric GSH levels, and decreased gastric MDA levels in ethanol-induced gastritis.
Conclusion and Discussion: Excessive alcohol consumption is considered one of the principal factors in gastric injuries. Investigations have also demonstrated that alcohol weakens the stomach's antioxidant/oxidant balance and prostaglandin (PG) synthesis. Our study demonstrated that RA significantly influences the preservation of gastric mucosal layer integrity and glands and impacts the protection of gastric ulcers in ethanol-induced gastritis. These effects may be due to the high antioxidant activity of RA and its role in raising PG secretion.
Methods and Materials: Animals were randomly divided into seven equal groups, six each, including a control group. After one hour of ethanol gavage, the animals received 50 mg/kg of sodium thiopental (intraperitoneal) and were sacrificed. The abdomen was exposed, and the stomach was removed.
Results: RA increased mucosal thickness, decreased gastric ulcers, enhanced the number of mucosal, chief, and parietal cells, decreased the presence of mucosal and submucosal leucocytes, reduced the number of gastric blood vessels in the mucosal and submucosal layers, increased gastric GSH levels, and decreased gastric MDA levels in ethanol-induced gastritis.
Conclusion and Discussion: Excessive alcohol consumption is considered one of the principal factors in gastric injuries. Investigations have also demonstrated that alcohol weakens the stomach's antioxidant/oxidant balance and prostaglandin (PG) synthesis. Our study demonstrated that RA significantly influences the preservation of gastric mucosal layer integrity and glands and impacts the protection of gastric ulcers in ethanol-induced gastritis. These effects may be due to the high antioxidant activity of RA and its role in raising PG secretion.
Type of Study: Congress |
Subject:
Related Fields
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
IBJ is a member of Committee on Publication Ethics (COPE)
and follows its guidelines |
The articles of this journal are licensed under
a Creative Commons Attribution-NonDerivatives 4.0 International License. .png) |
 IBJ is owned and published by Pasteur Institute of Iran |