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Neuroprotective Substances: Are they Able to Protect the Pancreatic Beta- Cells Too?
Rita U Ostrovskaya1, Sergei V Ivanov1
1V. Zakusov Research Institute of Pharmacology, 8, Baltiiskaya str., 125315, Moscow, Russia.
Background:
Growing pieces of evidence demonstrate a close relationship between type 2 diabetes (T2D) and neurodegenerative disorders such as Alzheimer's disease. The similarity of physiological and pathological processes occurring in pancreatic β-cells and neurons over the course of these pathologies allows raising the question of the practicability of studying neuroprotective substances for their potential antidiabetic activity.
Objective:
This review analyzes studies of antidiabetic and cytoprotective action on pancreatic β- cells of the neuroprotective compounds that can attenuate the oxidative stress and enhance the expression of neurotrophins: low-molecular-weight NGF mimetic compound GK-2, selective anxiolytic afobazole, antidepressants lithium chloride, and lithium carbonate on the rat streptozotocin model of T2D.
Results:
It was found that all the above-listed neuroprotective substances have a pronounced antidiabetic activity. The decrease in the β-cells number, the average area of the pancreatic islets, as well as the violation of their morphological structure caused by the streptozotocin was significantly weakened by the therapy with the investigated neuroprotective substances. The extent of these morphological changes clearly correlates with the antihyperglycemic effect of these compounds.
Conclusion:
The presented data indicate that the neuroprotective substances attenuating the damaging effect of oxidative stress and neurotrophins deficit cannot only protect neurons but also exert their cytoprotective effect towards pancreatic β-cells. These data may provide a theoretical basis for the further study of neuroprotective drugs as potential therapeutic options for T2D prevention and treatment.
Insights
Neuroprotective compounds show promise for treating type 2 diabetes (T2D). These substances protect pancreatic beta-cells from damage, suggesting a new therapeutic avenue for T2D prevention and management.
Area of Science:
- Endocrinology and Neuroscience
- Metabolic Disorders and Neurodegeneration
Background:
- Type 2 Diabetes (T2D) shares pathological pathways with neurodegenerative diseases.
- Pancreatic beta-cells and neurons exhibit similar vulnerabilities in these conditions.
Purpose of the Study:
- To review neuroprotective compounds for potential antidiabetic and cytoprotective effects on pancreatic beta-cells.
- To evaluate compounds like GK-2, afobazole, lithium chloride, and lithium carbonate in a rat T2D model.
Main Methods:
- Analysis of studies on neuroprotective agents in a rat streptozotocin-induced T2D model.
- Assessment of antidiabetic and cytoprotective actions, including oxidative stress attenuation and neurotrophin expression.
Main Results:
- All tested neuroprotective substances demonstrated significant antidiabetic activity.
- Therapy with these compounds mitigated streptozotocin-induced damage to beta-cells and pancreatic islets.
- Morphological improvements correlated with antihyperglycemic effects.
Conclusions:
- Neuroprotective agents can protect pancreatic beta-cells, similar to their neuronal protective effects.
- These findings support further investigation of neuroprotective drugs for T2D prevention and treatment.
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