Neuroprotective Effect of Cornus mas (cornelian cherry) on Global Cerebral Ischemia/Reperfusion Injury in Rats
Neuroprotective Effect of Cornus mas (cornelian cherry) on Global Cerebral Ischemia/Reperfusion Injury in Rats
Samira Asgharzade,1,*Masih Ameri,2Maryam Anjomshoa,3
1. 1- Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran 2- Department of Molecular Medicine, School of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran 2. Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran 3. Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran
Introduction: Ischemic stroke usually initiates inflammation and oxidative stress leading to neuronal death. Growing attention is currently being paid to the use of neuroprotective agents in ischemic strokes.
Cornelian cherry (Cornus mas L.) fruits are abundant in iridoids and anthocyanins—compounds with potent antioxidant and anti-inflammatory activity.
The study aims to evaluate the neuroprotective effect of Cornus mas L. extract (CME) on the cerebral ischemia/reperfusion injury (CIRI) model in rats and explore its potential anti-neuroinflammatory properties.
Methods: Fifty rats were randomly divided into five groups: sham, ischemia-reperfusion (I/R), 30 mg/kg CME, 60 mg/kg CME, and 120 mg/kg CME.
We used Middle cerebral artery occlusion (MCAO) to induction a rat CIRI model, different doses of CME were intraperitoneally injected 24 h after ischemia, for 14 days.
Histopathology assays were used to evaluate neurological damage and some inflammatory (Nitrite level (NO2-)), oxidative stress (malondialdehyde (MDA), and antioxidant power (ferric reducing antioxidant power (FRAP)) parameters were determined in the serum and hippocampus of rats by kit assay.
Results: The results of Hematoxylin and eosin staining showed that CME (30, 60, and 120 ml/kg) dose-dependently improved the CA3 diameter of the post-stroke pyramidal cell layers of the hippocampus but CA1 diameter was improved cell layers in 60 ml/kg dose.
CIRI significantly increased MDA and NO and decreased FRAP in the hippocampus and the serum levels in the ischemia group. However, the CME significantly declined the levels of MDA and NO and increased FRAP in the hippocampus and the serum levels in post-treatment groups.
Conclusion: Based on the findings, we concluded that CME has a neuroprotective potential against CIRI through antioxidant and anti-inflammatory properties and protects neurons against ischemic death.