Emerson de Oliveira Ferreira1, Mara Yone Soares Dias Fernandes2, Neila Maria Rocha de Lima3, Kelly Rose Tavares Neves4, Marta Regina Santos do Carmo5, Francisco Arnaldo Viana Lima6, Analu Aragão Fonteles7, Ana Paula Fontenele Menezes8, Geanne Matos de Andrade9. 1. Post-Graduate Programme in Medical Sciences, Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: emersonoliveira.shalom@hotmail.com. 2. Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: maraiony@hotmail.com. 3. Post-Graduate Programme in Medical Sciences, Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: neilamrl@hotmail.com. 4. Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: kelly.rose@hotmail.com. 5. Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: martacarmo@yahoo.com.br. 6. Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: arnviana@hotmail.com. 7. Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: analufonteless@gmail.com. 8. Post-Graduate Programme in Medical Sciences, Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceará, Brazil. Electronic address: ap_fontenele@yahoo.com.br. 9. Post-Graduate Programme in Medical Sciences, Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceará, Brazil; Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Brazil; Institute of Biomedicine of Brazilian Semi-arid, Brazil. Electronic address: gmatos@ufc.br.
Abstract
BACKGROUND: Cerebral ischemia is a common disease and one of the most common causes of death and disability worldwide. The lack of glucose and oxygen in neuronal tissue leads to a series of inflammatory events, culminating in neuronal death. Eriodictyol is a flavonoid isolated from the Chinese herb Dracocephalum rupestre that has been proven to have anti-inflammatory properties. HYPOTHESIS/ PURPOSE: Thus, the present study was designed to explore whether eriodictyol has neuroprotective effects against the neuronal damage, motor and memory deficits induced by permanent middle cerebral artery occlusion (pMCAO) in mice. STUDY DESIGN: Animals were orally treated with eriodictyol (1, 2 and 4mg/kg) or vehicle (saline) 30min before pMCAO, 2h after, and then once daily for the following five days. METHODS: The parameters studied were neuronal viability, brain infarcted area; sensorimotor deficits; exploratory activity; working and aversive memory; myeloperoxidase (MPO) activity; TNFα, iNOS and GFAP immunoreactivity. RESULTS: The treatment with eriodictyol prevented neuronal death, reduced infarct area and improved neurological and memory deficits induced by brain ischemia. The increase of MPO activity and TNF-α, iNOS and GFAP expression were also reduced by eriodictyol treatment. CONCLUSION: These findings demonstrate that eriodictyol exhibit promising neuroprotection effects against the permanent focal ischemia cerebral injury in the mice experimental model and the underlying mechanisms might be mediated through inhibition of neuroinflammation.
BACKGROUND:Cerebral ischemia is a common disease and one of the most common causes of death and disability worldwide. The lack of glucose and oxygen in neuronal tissue leads to a series of inflammatory events, culminating in neuronal death. Eriodictyol is a flavonoid isolated from the Chinese herb Dracocephalum rupestre that has been proven to have anti-inflammatory properties. HYPOTHESIS/ PURPOSE: Thus, the present study was designed to explore whether eriodictyol has neuroprotective effects against the neuronal damage, motor and memory deficits induced by permanent middle cerebral artery occlusion (pMCAO) in mice. STUDY DESIGN: Animals were orally treated with eriodictyol (1, 2 and 4mg/kg) or vehicle (saline) 30min before pMCAO, 2h after, and then once daily for the following five days. METHODS: The parameters studied were neuronal viability, brain infarcted area; sensorimotor deficits; exploratory activity; working and aversive memory; myeloperoxidase (MPO) activity; TNFα, iNOS and GFAP immunoreactivity. RESULTS: The treatment with eriodictyol prevented neuronal death, reduced infarct area and improved neurological and memory deficits induced by brain ischemia. The increase of MPO activity and TNF-α, iNOS and GFAP expression were also reduced by eriodictyol treatment. CONCLUSION: These findings demonstrate that eriodictyol exhibit promising neuroprotection effects against the permanent focal ischemia cerebral injury in the mice experimental model and the underlying mechanisms might be mediated through inhibition of neuroinflammation.
Authors: Zirong Deng; Sabba Hassan; Muhammad Rafiq; Hongshui Li; Yang He; Yi Cai; Xi Kang; Zhaoguo Liu; Tingdong Yan Journal: Evid Based Complement Alternat Med Date: 2020-12-12 Impact factor: 2.629