PROTECTIVE EFFECT OF MITOTEMPO IN STREPTOZOTOCIN-INDUCED DIABETIC RAT MODEL: EFFECTS ON CORPUS CAVERNOSUM AND AORTA
Objective: In this study we aimed to evaluate the effect of mitotempo, a mitochondria-specific antioxidant, on endothelial and erectile dysfunction in a Streptozotocin-induced rat diabetes model. Material and Methods: Wistar Albino rats weighing 280-320 g were used in the study. Diabetes was induced...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Istanbul University Press
2022-06-01
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| Series: | Sabiad |
| Subjects: | |
| Online Access: | https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/64A6AA95F5B6443CA8E9C6165870A354 |
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| Summary: | Objective: In this study we aimed to evaluate the effect of mitotempo, a mitochondria-specific antioxidant, on endothelial and erectile dysfunction in a Streptozotocin-induced rat diabetes model. Material and Methods: Wistar Albino rats weighing 280-320 g were used in the study. Diabetes was induced by intraperitoneal 50 mg/kg single dose streptozotocin injection. Blood glucose levels above 300 mg/dl at the end of 1 week were considered diabetes. Blood glucose was monitored for 4 weeks. The treatment group received mitotempo orally at 0.7 mg/kg/ day for 4 weeks. At the end of the 4th week, the aorta and corpus cavernosum contraction and relaxation responses were evaluated in an isolated organ bath after decapitation. Results: According to our study results, mitotempo 0.7 mg/kg/day for 4 weeks in a diabetes model preserved endothelial relaxation responses in both the thoracic aorta and corpus cavernosum. Phenylephrine contractions calculated according to KCl contraction did not differ between the groups. Conclusion: Endothelial cells can be identified as one of the first organs to be exposed to circulating substances. The effects of mROS on endothelial dysfunction caused by hyperglycemia is known. In our study, we found that a 0.7 mg/kg/day mitotempo treatment for 4 weeks showed protective effects on STZ-induced diabetic endothelial dysfunction. |
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| ISSN: | 2651-4060 |