Hydrogen sulphide protects H9c2 cells against chemical hypoxia-induced injury.
1. The aim of the present study was to investigate the effect of hydrogen sulphide (H(2)S) on cobalt chloride (CoCl(2))-induced injury in H9c2 embryonic rat cardiac cells. 2. After 36 h incubation in the presence of 600 micromol/L CoCl(2), reduced cell viability of H9c2 cells was observed, as well as the induction of apoptosis. In addition, CoCl(2) (600 micromol/L) enhanced the production of reactive oxygen species (ROS) and the expression of cleaved caspase 3, induced a loss of mitochondrial membrane potential (MMP) and decreased reduced glutathione (GSH) production. These results suggest that CoCl(2) induces similar responses to hypoxia/ischaemia. 3. Pretreatment of cells with 400 micromol/L NaHS (a H(2)S donor) for 30 min prior to exposure to CoCl(2) (600 micromol/L) significantly protected H9c2 cells against CoCl(2)-induced injury. Specifically, increased cell viability and decreased apoptosis were observed. In addition, NaHS pretreatment blocked the CoCl(2)-induced increases in ROS production and cleaved caspase 3 expression, as well as the decreases in GSH production and loss of MMP. 4. Pretreatment of cells with 2000 micromol/L N-acetylcysteine (NAC), a ROS scavenger, for 1 h prior to CoCl(2) exposure significantly protected H9c2 cells against CoCl(2)-induced injury, specifically enhancing cell viability, decreasing ROS production and preventing loss of MMP. 5. The findings of the present study suggest that H(2)S protects H9c2 cells against CoCl(2)-induced injury by suppressing oxidative stress and caspase 3 activation.
Chen
Si-Lin
SL
Department of Cardiovasology, Guangdong Provincial People's Hospital, Guangzhou, Guangdong, China.
Yang
Chun-Tao
CT
Yang
Zhan-Li
ZL
Guo
Rui-Xian
RX
Meng
Jin-Lan
JL
Cui
Yu
Y
Lan
Ai-Ping
AP
Chen
Pei-Xi
PX
Feng
Jian-Qiang
JQ
D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003035:Cobalt / Q000633:toxicity*; D019610:Cytoprotection / Q000187:drug effects* / Q000502:physiology*; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D009206:Myocardium / Q000166:cytology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D003035:Cobalt; C018021:cobaltous chloride; D006862:Hydrogen Sulfide