Cerebrolysin ameliorates prefrontal cortex and hippocampus neural atrophy of spontaneous hypertensive rats with hyperglycemia.
Leonardo Aguilar-HernándezMaria de Jesús Gómez-VillalobosGonzalo FloresPublished in: Synapse (New York, N.Y.) (2020)
Hyperglycemia of diabetes mellitus causes damage at the vascular level, which at the renal level represents diabetic nephropathy. In this pathology, there is arterial hypertension. In addition, several reports suggest that hyperglycemia and arterial hypertension affect interneuronal communication at the level of dendritic morphology. We studied these changes in an animal model with streptozotocin-induced diabetes mellitus in the spontaneous hypertensive (SH) rat. Recent reports from our laboratory have demonstrated that cerebrolysin (CBL), a preparation of neuropeptides with protective and repairing properties, reduces dendritic deterioration in both pathologies, in separate studies. In the present study, we evaluated the effect of CBL using the animal model with hyperglycemia and arterial hypertension and assessed the dendritic morphology using a Golgi-Cox staining procedure. Our results suggest that CBL ameliorated the reduction in the number of dendritic spines in the PFC and hippocampus caused by hyperglycemia in the SH rat. In addition, CBL also increased distal dendritic length in the PFC and hippocampus in hyperglycemic SH rats. Consequently, the CBL could be a therapeutic tool used to reduce the damage at the level of dendritic communication present in both pathologies.
Keyphrases
- arterial hypertension
- diabetic rats
- oxidative stress
- prefrontal cortex
- diabetic nephropathy
- blood pressure
- cerebral ischemia
- cognitive impairment
- minimally invasive
- adverse drug
- type diabetes
- high fat diet
- adipose tissue
- high resolution
- endothelial cells
- insulin resistance
- high glucose
- glycemic control
- subarachnoid hemorrhage