title: [Effect of hydrogen sulfide on oxidative stress and endoplasmic reticulum stress in diabetic cardiomyopathy].
abstract: OBJECTIVE
  To investigate the effects of hydrogen sulfide (H₂S) on oxidative stress and endoplasmic reticulum stress (ERS) in a rat model of diabetic cardiomyopathy (DCM).
  
  
  METHODS
  Thirty male SD rats were randomly divided into control group, diabetes group and treatment group( n = 10). Intraperitoneal injection of streptozotocin was utilized to establish a rat model of DCM. The rats with DCM in treatment group were intraperitoneally injected with NaHS solution. After treated for 12 weeks, the hearts isolated from rats were perfused on a langendorff apparatus. The ventricular hemodynamic parameters were measured. The ultrastructures of myocardium were observed using electron microscopy. The content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in myocardial tissue were determined by spectrophotometry. The expressions of C/EBP homologous protein( CHOP), glucose-regulated protein 78 (GRP78) and Caspase 12 at mRNA level in myocardium were detected using RT-PCR.
  
  
  RESULTS
  Compared with control group, the cardiac function and myocardial ultrastructure were damaged obviously in diabetic rats. In myocardial tissue, the content of MDA was increased, while the activities of SOD and GSH-Px were decreased. CHOP, GRP78 and Caspase 12 mRNA expressions were increased significantly. Compared with diabetes group, cardiac function and myocardial ultrastructure damage were improved in treatment group. The content of MDA was decreased, while the activities of SOD and GSH-Px were increased significantly. The mRNA levels of CHOP, GRP78 and Caspase 12 were increased.
  
  
  CONCLUSIONS
  H2S can protect myocardium in diabetic rats, maybe it is related to reduce oxidative stress damage and inhibition of the ERS-induced apoptosis pathway.
authors.forename: Rui
authors.initials: R
authors.lastname: Yang
authors.forename: Qiang
authors.initials: Q
authors.lastname: Jia
authors.forename: Xiao-fen
authors.initials: XF
authors.lastname: Liu
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Shan-feng
authors.initials: SF
authors.lastname: Ma
mesh_terms: D000818:Animals; D017209:Apoptosis; D053454:Caspase 12 / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D058065:Diabetic Cardiomyopathies / Q000188:drug therapy*; D059865:Endoplasmic Reticulum Stress; D005979:Glutathione Peroxidase / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000648:ultrastructure; D018384:Oxidative Stress; D051381:Rats; D013311:Streptozocin; D013482:Superoxide Dismutase / Q000378:metabolism; D051742:Transcription Factor CHOP / Q000378:metabolism; D000091342:Endoplasmic Reticulum Chaperone BiP
chemical_list: D053454:Caspase 12; D005979:Glutathione Peroxidase; D006360:Heat-Shock Proteins; D006862:Hydrogen Sulfide; D008315:Malondialdehyde; D013311:Streptozocin; D013482:Superoxide Dismutase; D051742:Transcription Factor CHOP; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP; C506443:Casp12 protein, rat