Neuroprotective Effects of Coriander and Garlic on Cerebellar Damage, Glial Activation and Synaptic Dysfunction in Diabetic Rats

Document Type : Original Article

Authors

1 Pathology department benha university

2 Department of Pathology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt.

3 Department of Pathology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt

Abstract

This study investigates neuroprotective effects of coriander seed extract (CSE) and garlic extract (GE) in alleviating these pathological changes in streptozotocin (STZ)-induced diabetic rat model. Adult male albino rats were given a single intraperitoneal injection of STZ (50 mg/kg) to induce diabetes. Diabetic rats were treated with CSE (250 mg/kg), GE (250 mg/kg), or glibenclamide (GLIB, 0.5 mg/kg) daily for 28 days. Cerebellar alterations, such as Purkinje cell count, glial fibrillary acidic protein (GFAP) expression, and synaptophysin expression, were evaluated by histopathological and immunohistochemical investigations. Additionally, the antioxidant ability (DPPH test) and total phenolic and flavonoid content of CSE and GE were assessed. STZ-induced diabetes resulted in a significant loss of Purkinje cells, increased GFAP expression indicative of reactive gliosis, and reduced synaptophysin expression, reflecting synaptic dysfunction. Treatment with CSE and GE significantly restored Purkinje cell numbers, reduced GFAP expression, and improved synaptophysin levels, with CSE demonstrating superior neuroprotective effects compared to GE and GLIB. The phytochemical analysis revealed that CSE contained higher phenolic content and comparable flavonoid content to GE, contributing to it powerful antioxidant and anti-inflammatory activities. CSE and GE exert neuroprotective effects by mitigating oxidative stress, reducing neuroinflammation, and preserving synaptic integrity in STZ-induced diabetic rats. These findings suggest their potential as natural therapeutic agents for managing diabetes-induced neurodegeneration.

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