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Protective Effect of Total Flavones of Abelmoschus manihot L. Medic Against Poststroke Depression Injury in Mice and Its Action Mechanism
Author(s) -
Liu Mei,
Jiang QiuHong,
Hao JiLi,
Zhou LanLan
Publication year - 2009
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.20864
Subject(s) - creb , pharmacology , glutathione peroxidase , superoxide dismutase , oxidative stress , malondialdehyde , lipid peroxidation , downregulation and upregulation , neuroprotection , chemistry , medicine , endocrinology , biochemistry , transcription factor , gene
Total flavones of Abelmoschus manihot L. Medic (TFA) is the major active component isolated from the traditional Chinese herb Abelmoschus manihot L. Medic. We investigated the protective effect of TFA against poststroke depression (PSD) injury in mice and its action mechanism. A mouse model of PSD was induced by middle cerebral artery occlusion (MACO) 30 min/reperfusion, followed by isolation feeding and chronic unpredictable mild stress for 2 weeks. Treatment groups received TFA at three different doses (160, 80, and 40 mg/kg, p.o.) or fluoxetine (Flu, 2.5 mg/kg, p.o.) daily for 24 days. Change in behavior, brain tissue malondialdehyde (MDA) levels, and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) were measured. The expression of brain‐derived neurotrophic factor (BDNF) was detected by immunohistochemistry, and mRNA expression of BDNF and cAMP response element‐binding protein (CREB) analyzed by reverse transcription‐polymerase chain reaction (RT‐PCR). Treatment with TFA (160, 80, and 40 mg/kg) significantly ameliorated mice escape‐directed behavioral impairment induced by PSD, markedly reduced MDA levels, and increased the activity of SOD, GSH‐Px close to normal levels. TFA administration also attenuated PSD‐induced neuronal death/losses, upregulated expression of BDNF both at mRNA and protein levels, as well as CREB mRNA levels. TFA had a protective effect against PSD injury in mice. Cardioprotection involves the inhibition of lipid peroxidation and upregulation of BDNF‐CREB levels in the hippocampus, which may also be important mechanism of its antidepressants. This potential protection makes TFA a promising therapeutic agent for the PSD. Anat Rec, 292:412–422, 2009. © 2009 Wiley‐Liss, Inc.