title: [Exogenous hydrogen sulfide protects against myocardial injury after skeletal muscle ischemia/reperfusion by inhibiting inflammatory cytokines and oxidative stress in rats].
abstract: OBJECTIVE
  To assess the protective effect of exogenous hydrogen sulfide (H₂S) against myocardial injury after skeletal muscle ischemia/reperfusion (IR) in rats and explore the mechanism.
  
  
  METHODS
  Thirty-one Wistar rats were randomized into normal control (n=8), IR group (n=8, with a 4-h reperfusion following a 4-h ischemia of the bilateral hindlimbs induced using a tourniquet), NaHS group (n=8, with IR and intraperitoneal injection of 14 µmol/kg NaHS), and DL-propargylglycine (PPG) group (n=7, with IR and intraperitoneal injection of 50 mg/kg PPG). The plasma levels of CK-MB and the levels of MPO, TNF-α, MDA, T-SOD, and CuZn-SOD in the plasma and myocardial tissues were measured. The expression of TNF-α in the myocardium was examined using immunohistochemistry. RESULTS Skeletal muscle IR induced significantly increased plasma CK-MB level (P<0.05) and the levels of MPO, TNF-α, and MDA in the plasma and myocardium, and significantly decreased plasma and myocardial levels of T-SOD and CuZn-SOD (P<0.05). NaHS treatment significantly decreased plasma CK-MB level (P<0.05), reduced plasma and myocardial levels of MPO, TNF-α, and MDA, and increased plasma and myocardial T-SOD and CuZn-SOD in rats with IR (P<0.05), whereas PPG treatment did not produce any obvious responses (P>0.05). Immunohistochemistry showed an obviously reduced expression of TNF-α in the myocardium in rats with NaHS treatment compared with those in IR group.
  
  
  CONCLUSIONS
  H₂S treatment can alleviate myocardial injury induced by skeletal muscle IR in rats by inhibiting the inflammatory cytokines and oxidative stress.
authors: Department Geriatric General Surgery, General Hospital of PLA, Beijing 100853, China. cw301@yahoo.cn
authors: Wen
authors: W
authors: Chen
authors: Ning
authors: N
authors: Liu
authors: Ying
authors: Y
authors: Zhang
authors: Yingchun
authors: Y
authors: Qi
authors: Jing
authors: J
authors: Yang
authors: Zhaoyang
authors: Z
authors: Deng
authors: Xiaoling
authors: X
authors: Li
authors: Xiaohua
authors: X
authors: Xie
mesh_terms: D000818:Animals; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D004195:Disease Models, Animal; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D007511:Ischemia / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D009195:Peroxidase; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form; D006862:Hydrogen Sulfide