Volume 11, Issue 3 (May & June 2020)                   BCN 2020, 11(3): 323-332 | Back to browse issues page

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Asgharzade S, Sewell R D E, Rabiei Z, Forouzanfar F, Kazemi Sheikhshabani S, Rafieian-Kopaei M. Hydroalcoholic Extract of Anchusa Italica Protects Global Cerebral Ischemia-Reperfusion Injury Via a Nitrergic Mechanism. BCN. 2020; 11 (3) :323-332
URL: http://bcn.iums.ac.ir/article-1-1425-en.html
1- Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
2- Cardiff School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff, CF10 3NB. Wales, U.K.
3- Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
4- Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Introduction: In stroke models, Inducible Nitric Oxide Synthase (iNOS) expression initiates cellular toxicity due to excessive Nitric Oxide (NO) generation. Anchusa italica is a medicinal herb with anti-inflammatory, antioxidant and neuroprotective properties. This study evaluated the antioxidant activity and NOS mRNA expression of the Hydroalcoholic Extract Of Anchusa Italica (HEAI) in an experimental stroke model in rats. 
Methods: The stroke model was induced by bilateral occlusion of both common carotid arteries for 60 min. Twenty-four hours after surgery, HEAI (50 and 100 mg/kg i.p.) was injected daily for 10 consecutive days. mRNA expression levels of NOS subtypes and hippocampal Brain-Derived Neurotrophic Factor (BDNF) were studied using real-time PCR. Besides, hippocampal tissue plus serum concentrations of NO and malondialdehyde (MDA) were measured.
Results: HEAI decreased MDA in both serum and hippocampal tissue and also reduced serum NO levels. Additionally, in the HEAI-treated groups, a down-regulation of iNOS mRNA expression, and an up-regulation of BDNF mRNA expression were observed.
Conclusion: The results indicated that the administration of HEAI even after the onset of ischemia protects the brain from free radical injury and inflammation via a down-regulation of iNOS expression inhibiting NO production and an up-regulation of BDNF mRNA.
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2019/02/11 | Accepted: 2019/07/20 | Published: 2020/05/1

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