PMID- 25376739
OWN - NLM
STAT- MEDLINE
DCOM- 20150817
LR  - 20181113
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 399
IP  - 1-2
DP  - 2015 Jan
TI  - Sodium hydrosulfide attenuates hyperhomocysteinemia rat myocardial injury through 
      cardiac mitochondrial protection.
PG  - 189-200
LID - 10.1007/s11010-014-2245-6 [doi]
AB  - Hydrogen sulfide (H2S) plays an important role during rat myocardial injury. 
      However, little is known about the role of H2S in hyperhomocysteinemia 
      (HHcy)-induced cardiac dysfunction as well as the underlying mechanisms. In this 
      study, we investigated whether sodium hydrosulfide (NaHS, a H2S donor) influences 
      methionine-induced HHcy rat myocardial injury in intact rat hearts and primary 
      neonatal rat cardiomyocytes. HHcy rats were induced by methionine (2.0 g/kg) and 
      the daily administration of 80 mumol/L NaHS in the HHcy + NaHS treatment group. At 
      the end of 4, 8, and 12 weeks, the ultrastructural alterations and functions of 
      the hearts were observed using transmission electron microscopy and 
      echocardiography system. The percentage of apoptotic cardiomyocytes, the 
      mitochondrial membrane potential, and the production of reactive oxygen species 
      (ROS) were measured. The expressions of cystathionine-gamma-lyase (CSE), Bax and 
      Bcl-2, caspase-3, phospho-endothelial nitric oxide synthase and the mitochondrial 
      NOX4 and cytochrome c were analyzed by Western blotting. The results showed the 
      cardiac dysfunction, the ultrastructural changes, and the apoptotic rate increase 
      in the HHcy rat hearts. In the primary neonatal rat cardiomyocytes of HHcy group, 
      ROS production was increased markedly, whereas the expression of CSE was 
      decreased. However, treatment with NaHS significantly improved the HHcy rat 
      hearts function, the ultrastructural changes, and decreased the levels of ROS in 
      the primary neonatal rat cardiomyocytes administrated with HHcy group. 
      Furthermore, NaHS down-regulated the expression of mitochondrial NOX4 and 
      caspase-3 and Bax and inhibited the release of cytochrome c from mitochondria. In 
      conclusion, H2S is involved in the attenuation of HHcy myocardial injury through 
      the protection of cardiac mitochondria.
FAU - Wang, Yuwen
AU  - Wang Y
AD  - Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin 
      Medical University, Harbin, 150086, Heilongjiang, China, yuww060424@hotmail.com.
FAU - Shi, Sa
AU  - Shi S
FAU - Dong, Shiyun
AU  - Dong S
FAU - Wu, Jichao
AU  - Wu J
FAU - Song, Mowei
AU  - Song M
FAU - Zhong, Xin
AU  - Zhong X
FAU - Liu, Yanhong
AU  - Liu Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141107
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Sulfides)
RN  - FWU2KQ177W (sodium bisulfide)
RN  - Homocysteinemia
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cardiotonic Agents/*pharmacology
MH  - Cells, Cultured
MH  - Drug Evaluation, Preclinical
MH  - Heart Diseases/prevention & control
MH  - Hyperhomocysteinemia/complications/*drug therapy
MH  - Male
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mitochondria, Heart/*drug effects/metabolism
MH  - Myocardium/pathology
MH  - Myocytes, Cardiac/drug effects/metabolism/physiology
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
MH  - Sulfides/*pharmacology
EDAT- 2014/11/08 06:00
MHDA- 2015/08/19 06:00
CRDT- 2014/11/08 06:00
PHST- 2014/07/19 00:00 [received]
PHST- 2014/10/09 00:00 [accepted]
PHST- 2014/11/08 06:00 [entrez]
PHST- 2014/11/08 06:00 [pubmed]
PHST- 2015/08/19 06:00 [medline]
AID - 10.1007/s11010-014-2245-6 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2015 Jan;399(1-2):189-200. doi: 10.1007/s11010-014-2245-6. Epub 
      2014 Nov 7.