PMID- 24286671
OWN - NLM
STAT- MEDLINE
DCOM- 20141024
LR  - 20140228
IS  - 1748-1716 (Electronic)
IS  - 1748-1708 (Linking)
VI  - 210
IP  - 3
DP  - 2014 Mar
TI  - L-3-n-Butylphthalide protects rats' cardiomyocytes from 
      ischaemia/reperfusion-induced apoptosis by affecting the mitochondrial apoptosis 
      pathway.
PG  - 524-33
LID - 10.1111/apha.12186 [doi]
AB  - AIMS: This study investigated the role of L-3-n-Butylphthalide (NBP) in cardiac 
      protection. METHODS: The left anterior descending coronary arteries (LAD) of the 
      rats were occluded for 30 min following by 2-h reperfusion to make the 
      ischaemia/reperfusion models. Neonatal cardiomyocytes were cultured and subjected 
      to hypoxia. L-3-n-Butylphthalide was administered intraperitoneally 2 h before 
      the surgery and right after the reperfusion in the in vivo experiments or added 
      to the culture medium in vitro. Haemodynamic parameters were recorded to evaluate 
      the cardiac functions, triphenyltetrazolium chloride (TTC) and Evens blue 
      staining were used to determine the area of risk and infarct area, apoptotic cell 
      numbers were counted with terminal deoxynucleotidyl transferase dUTP nick end 
      labelling (TUNEL) staining. Western blotting was used to determine the apoptotic 
      protein levels and immune staining to determine the translocation of 
      Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein. RESULTS: Our research 
      showed for the first time that L-3-n-Butylphthalide had great effects in 
      improving cardiac hemodynamic function and decreasing cardiac infarct areas and 
      apoptotic cell numbers in the peri-infarct areas. The apoptotic signals 
      investigation showed that L-3-n-Butylphthalide affected the mitochondrial pathway 
      including Bcl-2 protein expression, inhibition of caspase 3 activation and 
      cytochrome C releasing. Besides, Glyceraldehyde-3-phosphate dehydrogenase protein 
      translocation was inhibited by L-3-n-Butylphthalide treatment, and this effect 
      was mediated by endogenous reactive oxygen species (ROS). CONCLUSION: 
      L-3-n-Butylphthalide protects cardiomyocytes from ischaemia/reperfusion-induced 
      apoptosis by antioxidant effect and affecting mitochondrial apoptotic pathway.
CI  - (c) 2013 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.
FAU - Wang, Y-G
AU  - Wang YG
AD  - Neurology Department of Shanghai Renji Hospital Affiliated to Jiaotong 
      University, Shanghai, China.
FAU - Li, Y
AU  - Li Y
FAU - Wang, C-Y
AU  - Wang CY
FAU - Ai, J-W
AU  - Ai JW
FAU - Dong, X-Y
AU  - Dong XY
FAU - Huang, H-Y
AU  - Huang HY
FAU - Feng, Z-Y
AU  - Feng ZY
FAU - Pan, Y-M
AU  - Pan YM
FAU - Lin, Y
AU  - Lin Y
FAU - Wang, B-X
AU  - Wang BX
FAU - Yao, L-L
AU  - Yao LL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131129
PL  - England
TA  - Acta Physiol (Oxf)
JT  - Acta physiologica (Oxford, England)
JID - 101262545
RN  - 0 (Antioxidants)
RN  - 0 (Benzofurans)
RN  - 0 (Reactive Oxygen Species)
RN  - 822Q956KGM (3-n-butylphthalide)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Benzofurans/*pharmacology
MH  - Blotting, Western
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Mitochondria/drug effects/metabolism/pathology
MH  - Myocardial Reperfusion Injury/metabolism/pathology/*prevention & control
MH  - Myocytes, Cardiac/*drug effects/metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species
OTO - NOTNLM
OT  - L-3-n-butylphthalide
OT  - apoptosis
OT  - cardiomyocyte
OT  - infarction
EDAT- 2013/11/30 06:00
MHDA- 2014/10/25 06:00
CRDT- 2013/11/30 06:00
PHST- 2013/07/05 00:00 [received]
PHST- 2013/07/24 00:00 [revised]
PHST- 2013/10/21 00:00 [revised]
PHST- 2013/10/22 00:00 [accepted]
PHST- 2013/11/30 06:00 [entrez]
PHST- 2013/11/30 06:00 [pubmed]
PHST- 2014/10/25 06:00 [medline]
AID - 10.1111/apha.12186 [doi]
PST - ppublish
SO  - Acta Physiol (Oxf). 2014 Mar;210(3):524-33. doi: 10.1111/apha.12186. Epub 2013 
      Nov 29.