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Neuroprotective Dipeptide Noopept Prevents DNA Damage in Mice with Modeled Prediabetes
R U Ostrovskaya1, S S Yagubova2, A K Zhanataev2
1V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia. rita.ostrovskaya@gmail.com.
Abstract:
In experiments on BALB/c mice, prediabetes was modeled by administration of streptozotocin in a dose of 130 mg/kg. DNA damage was assessed by the method of DNA comets. Noopept (0.5 mg/kg intraperitoneally) was administered for 14 days before and for 6, 13, or 14 days after streptozotocin administration. Despite moderate hyperglycemia and increased malondialdehyde level, the intensity of DNA damage in cells of the pancreas, liver, and kidneys significantly surpassed the control values. Noopept normalized these parameters due to its pronounced antigenotoxic effect. For both the damaging effect of streptozotocin and the normalizing effect of Noopept, DNA changes manifested mainly in terms of atypical DNA comets. Our findings confirm the role of DNA damage in the pathogenesis of diabetes. They indicate the possibility of pharmacological protection of pancreatic β cells with the neuroprotective drug and provide an important argument in favor of the hypothesis about the similarity of the mechanisms of formation of the resistance of neurons and β cells to the cytotoxic influences.
Insights
This study shows that the neuroprotective drug Noopept can prevent DNA damage in key organs during prediabetes, offering a potential way to protect pancreatic beta cells.
Area of Science:
- Biomedical Science
- Toxicology
- Pharmacology
Background:
- Prediabetes involves significant cellular damage, particularly DNA damage, in organs like the pancreas, liver, and kidneys.
- Streptozotocin administration is a common method for modeling prediabetes and inducing hyperglycemia and oxidative stress.
Purpose of the Study:
- To investigate the antigenotoxic effects of Noopept in a prediabetes model.
- To assess the potential of Noopept in protecting pancreatic beta cells and other organs from streptozotocin-induced DNA damage.
Main Methods:
- BALB/c mice were induced into a prediabetic state using streptozotocin (130 mg/kg).
- DNA damage was quantified using the DNA comet assay.
- Noopept (0.5 mg/kg) was administered pre- and post-streptozotocin exposure.
Main Results:
- Streptozotocin induced moderate hyperglycemia, increased malondialdehyde levels, and significant DNA damage in pancreatic, liver, and kidney cells.
- Noopept administration effectively normalized these parameters, demonstrating a pronounced antigenotoxic effect.
- DNA changes, characterized by atypical DNA comets, were observed following both streptozotocin damage and Noopept's protective action.
Conclusions:
- DNA damage plays a crucial role in the pathogenesis of diabetes.
- Noopept exhibits potential for the pharmacological protection of pancreatic beta cells.
- The findings support the hypothesis of similar resistance mechanisms in neurons and beta cells against cytotoxic influences.
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