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  4. Honokiol, a neuroprotectant against mouse cerebral ischaemia, mediated by preserving Na+, K+-ATPase activity and mitochondrial functions
 
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Honokiol, a neuroprotectant against mouse cerebral ischaemia, mediated by preserving Na+, K+-ATPase activity and mitochondrial functions

Journal
Basic and Clinical Pharmacology and Toxicology
Journal Volume
101
Journal Issue
2
Pages
108-116
Date Issued
2007
Author(s)
CHANG-MU CHEN  
Liu S.-H.
Lin-Shiau S.-Y.
DOI
10.1111/j.1742-7843.2007.00082.x
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-34447636627&doi=10.1111%2fj.1742-7843.2007.00082.x&partnerID=40&md5=6b61f3af78b2fe2d89f8a8085e2a7ab0
https://scholars.lib.ntu.edu.tw/handle/123456789/476293
Abstract
Honokiol, a component of the herb Magnolia officinalis, exhibits antioxidant, anti-inflammatory and anxiolytic properties, increases seizure threshold, and promotes neurite outgrowth. Because stroke has become the second leading cause of death in industrialized countries, an effective neuroprotectant is urgently required. In this study, we attempted to elucidate in a mouse cerebral ischaemia model whether honokiol could be a neuroprotectant. Adult male Institute of Cancer Research (ICR) mice were subjected to middle cerebral artery occlusion for 45 min. Honokiol (10 μg/kg in 0.2 ml of saline) or control vehicle was intraperitoneally administered twice, 15 min. before and 60 min. after the induction of ischaemia. Cerebral ischaemia induced by this method was associated with an increase in synaptosomal production of reactive oxygen species, with decreases in synaptosomal mitochondrial membrane potential (ΔΨm) and synaptosomal mitochondrial metabolic function, and with reductions in Na+, K+-ATPase activities of tissues isolated from selected brain regions. Administration of honokiol resulted in significant reductions in brain infarct volume and in synaptosomal production of reactive oxygen species. The decreases in synaptosomal mitochondrial membrane potential, synaptosomal mitochondrial metabolic function and tissue Na +, K+-ATPase activities observed in the ischaemic brains were also attenuated by honokiol treatments. It is concluded that honokiol can protect brain against ischaemic reperfusion injury and preserve mitochondrial function from oxidative stress. Regarding therapeutic application, further studies are needed to assess the efficacy and safety of honokiol in clinical situations. ? 2007 The Authors.
SDGs

[SDGs]SDG3

Other Subjects
adenosine triphosphatase (potassium sodium); adenosine triphosphatase (potassium); honokiol; neuroprotective agent; sodium chloride; animal experiment; animal model; article; brain ischemia; controlled study; enzyme activity; enzyme inhibition; Institute for Cancer Research mouse; male; membrane potential; middle cerebral artery occlusion; mitochondrial membrane; mitochondrion; mouse; neuroprotection; nonhuman; priority journal; Animals; Anti-Anxiety Agents; Biphenyl Compounds; Brain Ischemia; Lignans; Male; Membrane Potential, Mitochondrial; Mice; Mice, Inbred ICR; Na(+)-K(+)-Exchanging ATPase; Neuroprotective Agents; Reactive Oxygen Species; Synaptosomes; Magnolia officinalis; Mus
Type
journal article

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