期刊论文详细信息
Basic and Clinical Neuroscience
Hydroalcoholic Extract of Anchusa Italica Protects Global Cerebral Ischemia-Reperfusion Injury Via a Nitrergic Mechanism
ARTICLE
Asgharzade, Samira1  Sewell, Robert D. E.2  Rabiei, Zahra3  Forouzanfar, Fatemeh4  Kazemi Sheikhshabani, Sedigheh1  Rafieian-Kopaei, Mahmoud3 
[1] Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences;Cardiff School of Pharmacy and Pharmaceutical Sciences, Cardiff University;Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences;Neuroscience Research Center, Mashhad University of Medical Sciences
关键词: Anchusa italica;    Ischemia-reperfusion;    Nitric oxide;    Stroke;   
DOI  :  10.32598/bcn.11.2.1665.2
来源: Iran University of Medical Sciences
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【 摘 要 】

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.

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