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1- Department of Anatomical Sciences, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran
2- Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
3- Department of Physiology and Pharmacology, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran
4- Department of Neuroscience, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran
Abstract:  
Alzheimerchr('39')s disease (AD) is a complex neurodegenerative disorder with a progressive template leading to neural damage as well as cognitive and memory deficit. The present study designed to investigate the neuroprotective effects of Centella Asiatica (CA) in STZ-induced rat model of memory impairment and neuronal damage. ICV infusion of STZ (3 mg/kg) or saline (as vehicle) were performed on days 1 and 3. CA (150 and 300 mg/kg/day) was administered through oral gavage for 21 days after model induction. Y-maze test was carried out to assess working memory related performances of animals. Rats were then sacrificed and the hippocampi were harvested for evaluation of neuronal density in CA1, CA2, CA3, and DG regions using stereology technique. ICV infusion of STZ caused significant working memory impairment in Y-maze apparatus as indicated with a significant decrease in alternative behavior compared to control animals (40.67 ± 2.04 vs. 73.00 ± 1.88, p < 0.0001). Oral administration of CA (150 and 300 mg/kg each day) for 21 days significantly (55.33 ± 3.34 and 57.17 ± 3.81 vs. 40.67 ± 2.04, p < 0.013, p < 0.004) improved STZ-induced working memory deficit. Furthermore, 21 days consecutive administration of CA significantly ameliorated STZ-induced neuronal loss in the CA1, CA2, and DG subfields of the hippocampus. Overall, these data demonstrate that CA increases neuronal density and improves cognitive impairment in STZ- induced rat model of AD, thereby has a promising therapeutic potential for neurodegenerative disorders. Accordingly, further studies are needed to determine the exact molecular mechanism of CA protective effects in brain disorders particularly AD
Type of Study: Original | Subject: Behavioral Neuroscience
Received: 2020/02/5 | Accepted: 2020/06/29

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