Prof. Dr. Ertuğrul Kılıç. Vet. Hek. Musa Ekrem Özdemir ve Yük. Mak. Tek. Ali Şenbahçe'ye desteklerinden dolayı teşekkür ederiz.
Objective: Chronic stress plays an important role in the etiology of many inflammatory diseases. Reactive oxygen species (ROS), a source of free radicals, act as signaling molecules in the progression of stress-related inflammatory diseases. Oxidative stress occurs as a result of an increase in free radicals in the tissues. The damage caused by oxidative stress can be reduced by antioxidant replacement. In our study, the effect of fulvic acid, a powerful antioxidant, on the damage caused by the water avoidance stress model in the rat colon was investigated morphologically and biochemically.
Methods: Experimental groups (n=6, Sprague-Dawley male rats, 300 g): control (C), water avoidance stress (WAS), and water avoidance stress+fulvic acid (WAS+FA). Rats in the WAS + FA group were given a single dose of FA (150 mg/kg i.p.) immediately after exposure to water avoidance stress. The colons were stained with hematoxylin-eosin and toluidine blue. Total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were analyzed biochemically.
Results: Compared to the C group, the WAS group showed epithelial damage, a few empty goblet cells, inflammatory cell infiltration, and many active mast cells in the connective tissue. Mucosal integrity, the number of goblet cells, and mast cell activity improved in the WAS+FA group as compared to the WAS group. Biochemically, as compared to the C group, TAS levels decreased, and TOS and OSI levels increased in the WAS group. In the WAS+FA group, TAS levels increased, and TOS and OSI levels decreased with respect to those in the WAS group.
Conclusion: Our findings indicated that fulvic acid reduced the damage caused by chronic oxidative stress in the colon.
Primary Language | English |
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Subjects | Health Care Administration |
Journal Section | Articles |
Authors | |
Publication Date | March 28, 2023 |
Submission Date | January 29, 2022 |
Published in Issue | Year 2023 Volume: 13 Issue: 1 |