PMID- 22453521
OWN - NLM
STAT- MEDLINE
DCOM- 20121105
LR  - 20211021
IS  - 1573-6903 (Electronic)
IS  - 0364-3190 (Linking)
VI  - 37
IP  - 8
DP  - 2012 Aug
TI  - Naringin treatment improves functional recovery by increasing BDNF and VEGF 
      expression, inhibiting neuronal apoptosis after spinal cord injury.
PG  - 1615-23
LID - 10.1007/s11064-012-0756-7 [doi]
AB  - The aim of this study was to determine the therapeutic efficacy of starting 
      naringin treatment 1 day after spinal cord injury (SCI) in rat and to investigate 
      the underlying mechanism. SCI was induced using the modified weight-drop method 
      in Sprague-Dawley rats. The SCI animals were randomly divided into three groups: 
      vehicle-treated group; 20 mg/kg naringin-treated group; 40 mg/kg naringin-treated 
      group, and additionally with sham group (laminectomy only). Locomotors functional 
      recovery was assessed during the 6 weeks post operation period by performing 
      open-field locomotors tests and inclined-plane tests. At the end of the study, 
      the segments of spinal cord encompassing the injury site were removed for 
      histopathological analysis. Immunohistochemistry was performed to observe the 
      expression of the brain-derived neurotrophic factor (BDNF). The expression of 
      vascular endothelial growth factor (VEGF), B-cell CLL/lymphoma-2 (Bcl-2), 
      BCL-2-associated X protein (Bax) and caspase-3 were detected by Western blot 
      analysis. The apoptotic neural cells were assessed using the TUNEL method. The 
      results showed that the naringin-treated animals had significantly better 
      locomotor function recovery, less myelin loss, and higher expression of BDNF and 
      VEGF. In addition, naringin treatment significantly increased in Bcl-2:Bax ratio, 
      reduced the enzyme activity of caspase-3 and decreased the number of apoptotic 
      cells after SCI. These findings suggest that naringin treatment starting 1 day 
      after SCI can significantly improve locomotor recovery, and this neuroprotective 
      effect may be related to the upregulation of BDNF and VEGF and the inhibition of 
      neural apoptosis. Therefore, naringin may be useful as a promising therapeutic 
      agent for SCI.
FAU - Rong, Wei
AU  - Rong W
AD  - Department of Orthopedics, Peking University Third Hospital, Beijing, China.
FAU - Wang, Jun
AU  - Wang J
FAU - Liu, Xiaoguang
AU  - Liu X
FAU - Jiang, Liang
AU  - Jiang L
FAU - Wei, Feng
AU  - Wei F
FAU - Hu, Xing
AU  - Hu X
FAU - Han, Xiaoguang
AU  - Han X
FAU - Liu, Zhongjun
AU  - Liu Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120328
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Caspase Inhibitors)
RN  - 0 (Flavanones)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (bcl-2-Associated X Protein)
RN  - N7TD9J649B (naringin)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/biosynthesis
MH  - Caspase Inhibitors
MH  - Female
MH  - Flavanones/administration & dosage/*therapeutic use
MH  - Motor Activity/drug effects
MH  - Myelin Sheath/drug effects
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Recovery of Function/drug effects
MH  - Spinal Cord Injuries/drug therapy/*physiopathology
MH  - Vascular Endothelial Growth Factor A/biosynthesis
MH  - bcl-2-Associated X Protein
EDAT- 2012/03/29 06:00
MHDA- 2012/11/06 06:00
CRDT- 2012/03/29 06:00
PHST- 2011/12/12 00:00 [received]
PHST- 2012/03/16 00:00 [accepted]
PHST- 2012/03/13 00:00 [revised]
PHST- 2012/03/29 06:00 [entrez]
PHST- 2012/03/29 06:00 [pubmed]
PHST- 2012/11/06 06:00 [medline]
AID - 10.1007/s11064-012-0756-7 [doi]
PST - ppublish
SO  - Neurochem Res. 2012 Aug;37(8):1615-23. doi: 10.1007/s11064-012-0756-7. Epub 2012 
      Mar 28.