PMID- 18949543
OWN - NLM
STAT- MEDLINE
DCOM- 20090511
LR  - 20161020
IS  - 1573-7241 (Electronic)
IS  - 0920-3206 (Linking)
VI  - 23
IP  - 2
DP  - 2009 Apr
TI  - Poly (ADP-ribose) polymerase inhibition improves endothelial dysfunction induced 
      by hyperhomocysteinemia in rats.
PG  - 121-7
LID - 10.1007/s10557-008-6146-3 [doi]
AB  - INTRODUCTION: We investigated the possible protective effect of poly (ADP-ribose) 
      polymerase (PARP) inhibition in preventing endothelial dysfunction induced by 
      hyperhomocysteinemia (Hhcy). METHODS: Sprague-Dawley rats were divided into Hhcy 
      group, Hhcy + 3-aminobenzamide(3-AB) group, control group and control + 3-AB 
      group. A high-methionine diet was given to induce hyperhomocysteinemia. In Hhcy + 
      3-AB and control + 3-AB groups, rats were injected intraperitoneally with 3-AB 
      (inhibitor of PARP). After 45 days, ultrastructural changes of aortas were 
      observed by transmission electron microscope. Vascular reactivity of thoracic 
      aortic rings was measured in organ chambers. PARP activity was detected. The 
      levels of plasma total homocysteine, nitrite/nitrate, endothelin (ET)-1 and 
      malondialdehyde were assayed. RESULTS: Rats in Hhcy group developed severe 
      hyperhomocysteinemia and significant loss of endothelial function as measured by 
      both vascular rings and levels of nitrite/nitrate and ET-1. Malondialdehyde 
      levels increased significantly in Hhcy rats compared with control rats. 3-AB 
      improved Ach-induced, NO-mediated vascular relaxation and stabilized the level of 
      nitrite/nitrate and ET-1. Obvious improvement of ultrastructure can be observed 
      in Hhcy + 3-AB group. CONCLUSIONS: These results suggest that pharmacological 
      inhibition of PARP prevents the development of endothelial dysfunction in rats 
      with hyperhomocysteinemia which may represent a novel approach to improve 
      vascular dysfunction associated with hyperhomocysteinemia.
FAU - Yu, Xian
AU  - Yu X
AD  - Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430022, China.
FAU - Cheng, Xiang
AU  - Cheng X
FAU - Xie, Jiang-jiao
AU  - Xie JJ
FAU - Liao, Meng-yang
AU  - Liao MY
FAU - Yao, Rui
AU  - Yao R
FAU - Chen, Yong
AU  - Chen Y
FAU - Ding, Ying-jun
AU  - Ding YJ
FAU - Tang, Ting-ting
AU  - Tang TT
FAU - Liao, Yu-hua
AU  - Liao YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081024
PL  - United States
TA  - Cardiovasc Drugs Ther
JT  - Cardiovascular drugs and therapy
JID - 8712220
RN  - 0 (Benzamides)
RN  - 0 (Endothelin-1)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Poly(ADP-ribose) Polymerase Inhibitors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - 8J365YF1YH (3-aminobenzamide)
SB  - IM
MH  - Animals
MH  - Aorta, Thoracic/drug effects/pathology
MH  - Benzamides/*pharmacology
MH  - Disease Models, Animal
MH  - Endothelin-1/drug effects/metabolism
MH  - Endothelium, Vascular/drug effects/physiopathology
MH  - Enzyme Inhibitors/*pharmacology
MH  - Hyperhomocysteinemia/*drug therapy/physiopathology
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Microscopy, Electron, Transmission
MH  - Nitric Oxide/metabolism
MH  - Oxidative Stress/drug effects
MH  - *Poly(ADP-ribose) Polymerase Inhibitors
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2008/10/25 09:00
MHDA- 2009/05/12 09:00
CRDT- 2008/10/25 09:00
PHST- 2008/02/20 00:00 [received]
PHST- 2008/10/02 00:00 [accepted]
PHST- 2008/10/25 09:00 [pubmed]
PHST- 2009/05/12 09:00 [medline]
PHST- 2008/10/25 09:00 [entrez]
AID - 10.1007/s10557-008-6146-3 [doi]
PST - ppublish
SO  - Cardiovasc Drugs Ther. 2009 Apr;23(2):121-7. doi: 10.1007/s10557-008-6146-3. Epub 
      2008 Oct 24.