PMID- 19248161
OWN - NLM
STAT- MEDLINE
DCOM- 20090519
LR  - 20131121
IS  - 1932-8494 (Electronic)
IS  - 1932-8486 (Linking)
VI  - 292
IP  - 3
DP  - 2009 Mar
TI  - Protective effect of total flavones of Abelmoschus manihot L. Medic against 
      poststroke depression injury in mice and its action mechanism.
PG  - 412-22
LID - 10.1002/ar.20864 [doi]
AB  - 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.
CI  - (c) 2009 Wiley-Liss, Inc.
FAU - Liu, Mei
AU  - Liu M
AD  - Department of Pharmacology, Basic Medical College, Anhui Medical University, 
      Hefei, People's Republic of China.
FAU - Jiang, Qiu-Hong
AU  - Jiang QH
FAU - Hao, Ji-Li
AU  - Hao JL
FAU - Zhou, Lan-Lan
AU  - Zhou LL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Anat Rec (Hoboken)
JT  - Anatomical record (Hoboken, N.J. : 2007)
JID - 101292775
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Flavones)
RN  - 0 (RNA, Messenger)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Abelmoschus/*chemistry
MH  - Animals
MH  - Behavior, Animal
MH  - Brain Injuries/*drug therapy/metabolism
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/genetics/metabolism
MH  - Depressive Disorder/*drug therapy/metabolism
MH  - Drugs, Chinese Herbal/*therapeutic use
MH  - Flavones/*therapeutic use
MH  - Glutathione Peroxidase/metabolism
MH  - Hippocampus/drug effects
MH  - Infarction, Middle Cerebral Artery/chemically induced/complications
MH  - Lipid Peroxidation
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Mice
MH  - *Phytotherapy
MH  - RNA, Messenger/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stroke/etiology/*pathology
MH  - Superoxide Dismutase/metabolism
EDAT- 2009/02/28 09:00
MHDA- 2009/05/20 09:00
CRDT- 2009/02/28 09:00
PHST- 2009/02/28 09:00 [entrez]
PHST- 2009/02/28 09:00 [pubmed]
PHST- 2009/05/20 09:00 [medline]
AID - 10.1002/ar.20864 [doi]
PST - ppublish
SO  - Anat Rec (Hoboken). 2009 Mar;292(3):412-22. doi: 10.1002/ar.20864.