Introduction: Acrylamide is a synthetic chemical compound commonly used in many branches of industry. Researchers have found acrylamide in certain foods that were heated to a temperature above 120°C. Ginseng is a widely used herbal medicine with numerous beneficial effects. Ginseng is suggested to contribute to a protective effect in neurodegenerative disorders.
Aim of the study: The aim of the present study was to evaluate the possible protective effect of ginseng against the midbrain injury induced by acrylamide in adult male albino rats.
Materials and methods: A total of 35 adult male albino rats were used. They were divided into three groups. Group I (15 animals) was allowed water ad libitum and fed a standard diet (control). Group II (10 animals) was given acrylamide orally by means of a gastric tube daily at a dose of 30 mg/kg for 4 weeks. Group III (10 animals) was given acrylamide daily at the same dissolution, dose, route and duration as group II concomitantly with ginseng solution through a gastric tube at a dose of 20 mg/kg. Samples from the brainstem were taken and processed for light and electron microscopic investigation.
Results: Light microscopic examination of the midbrain of the acrylamide-treated animals showed signs of injury. Glial fibrillary acidic protein-positive cells were more abundant in the midbrain of treated animals compared with control animals. Ultrastructural study of the midbrain of the acrylamide-treated group showed dilated RER in association with mitochondria with destroyed cristae. Many myelinated nerve fibers showed degenerative changes. These structural changes were much less pronounced in animals concomitantly treated with acrylamide and ginseng.
Conclusion: Ginseng can reduce the severity of the injurious effects induced by acrylamide.
Histology Department, Faculty of Medicine, Tanta University, Tanta, Egypt
Correspondence to Essam M. Laag, MD, Histology Department, Faculty of Medicine, Tanta University, Tanta, Egypt Tel: +20 122 048 8500; e-mail: email@example.com
Received November 5, 2013
Accepted March 24, 2014