Volume 46, Issue 3 (9-2022)
Research in Medicine 2022, 46(3): 60-72 |
Back to browse issues page
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran. , eidi@srbiau.ac.ir
Abstract: (798 Views)
Background and Aim: Gastric ulcer is a chronic gastrointestinal disease caused by the use of nonsteroidal anti-inflammatory drugs (NSAIDs) that increase the risk of gastrointestinal complications, such as ulcers or bleeding. The use of antioxidants as adjunctive therapy for this disease is very important. Pantothenic acid is a B vitamin and a powerful antioxidant that plays an important role in the metabolism of carbohydrates, fats, and proteins in the body. The aim of the present study was to evaluate the effect of pantothenic acid on antioxidant factors in improving experimental models of indomethacin-induced gastric ulcer in NMRI mice.
Methods: In the current experimental study, 60 adult male NMRI mice (body weight: 25-30 g) were randomly divided into 10 groups. Mice in the control group were intact. The sham group received pantothenic acid solvent (normal saline). The experimental groups received pantothenic acid at doses of 100, 200, and 400 mg/kg, omeprazole (40 mg/kg) as standard drug and indomethacin (18 mg/kg) to induce ulcers by gavage for two weeks. Six hours after receiving indomethacin and wounding, the mice's stomachs were examined for macroscopic evaluation of the ulcer at the epithelial level, visible lesions, inflammation with bleeding, and edema as well as biochemical evaluation of antioxidant enzymes by light absorption using an ELISA device. Statistical data were analyzed running one-way ANOVA.
Results: Administration of indomethacin significantly reduces gastric antioxidants, such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity (p<0.001), and increases malondialdehyde (MDA) levels as compared with the normal control group (p<0.001). Treatment with pantothenic acid significantly increased the amount of SOD and CAT with doses of 200 (p<0.01), 400 mg/kg (p<0.001), and GPx in both doses (p<0.001) and the level of MDA with doses of 200 (p<0.05) and 400 mg/kg (p<0.001) significantly decreased. The result of pantothenic acid was 400 mg/kg equivalent to omeprazole and no significant difference was observed between the two substances.
Conclusion: The results of our study suggest that pantothenic acid can protect the stomach against indomethacin-induced ulceration in mice.
Methods: In the current experimental study, 60 adult male NMRI mice (body weight: 25-30 g) were randomly divided into 10 groups. Mice in the control group were intact. The sham group received pantothenic acid solvent (normal saline). The experimental groups received pantothenic acid at doses of 100, 200, and 400 mg/kg, omeprazole (40 mg/kg) as standard drug and indomethacin (18 mg/kg) to induce ulcers by gavage for two weeks. Six hours after receiving indomethacin and wounding, the mice's stomachs were examined for macroscopic evaluation of the ulcer at the epithelial level, visible lesions, inflammation with bleeding, and edema as well as biochemical evaluation of antioxidant enzymes by light absorption using an ELISA device. Statistical data were analyzed running one-way ANOVA.
Results: Administration of indomethacin significantly reduces gastric antioxidants, such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity (p<0.001), and increases malondialdehyde (MDA) levels as compared with the normal control group (p<0.001). Treatment with pantothenic acid significantly increased the amount of SOD and CAT with doses of 200 (p<0.01), 400 mg/kg (p<0.001), and GPx in both doses (p<0.001) and the level of MDA with doses of 200 (p<0.05) and 400 mg/kg (p<0.001) significantly decreased. The result of pantothenic acid was 400 mg/kg equivalent to omeprazole and no significant difference was observed between the two substances.
Conclusion: The results of our study suggest that pantothenic acid can protect the stomach against indomethacin-induced ulceration in mice.
Type of Study: Original |
Subject:
Physilogy
Received: 2021/07/27 | Accepted: 2022/03/6 | Published: 2023/01/2
Received: 2021/07/27 | Accepted: 2022/03/6 | Published: 2023/01/2
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |