Cerebrolysin attenuates diabetic–induced sympathy in hippocampus of albino rats

Document Type : Original Article

Authors

1 Department of Anatomy and Embryology, College of Medicine, Mansoura University

2 Department of Physiology, College of Medicine, Mansoura University

3 anatomy department, faculty of medicine, Mansoura university, Mansoura, Egypt

4 Department of anatomy,Faculty of medicine,Mansoura university

5 Anatomy department,faculty of medicine,ain shams university

6 Department of Neurology, college of medicine, Benha University

Abstract

ABSTRACT
Background: Cognitive dysfunction is one of the central nervous system complications of diabetes. Aim of work: the aim of the present study is to investigate cerebrolycin (Cbl) therapy neuroprotective influence on synaptopathy that diabetes causes in the hippocampus. Material and Methods: Twenty four male albino rats were randomly distributed among four groups (each group 6 rats); control, diabetic, cerebrolysin (Cbl) and diabetic administered cerebrolysin (diabetes+Cbl). Part of cerebrum of rats were taken after 8 weeks from all groups and the samples were collected for histological and histochemical evaluation using cresyl violet ,hematoxylin and eosin and immunohistochemical staining with glial fibillary acidic protein (GFAP) for fibrosis, synaptophysin for synaptogenesis evaluation. Results: Treatment of streptozotocin-induced diabetic rats with cerebrolysin showed minimal pathological changes than that reported in the diabetic group as detected by mild neuronal injury in the granular layer of the Cornu Ammonis and normal molecular layer. Cresyl violet stain showed mild increase in Nissl granules but less than in the control group. Moreover, diabetic rats receiving Cbl showed significant decrease in the area fraction of GFA immunoreactivity but have significant increase in Synaptophysin manifestation. Conclusions: Cerebrolysin has the ability to protect against changes caused by diabetes in the hippocampus through reducing gliosis but significantly improving cognitive dysfunction by improving synopathy.

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