title: Cystamine ameliorates ventricular hypertrophy associated with modulation of IL-6-mediated signaling in lupus-prone mice.
abstract: OBJECTIVE
  The aim of this study is to investigate the protective effects of cystamine on lupus-associated cardiac hypertrophy.
  
  
  METHODS
  Balb/c and lupus-prone NZB/W-F1 mice were individually randomized into sham group (saline, n=16) and cystamine group (n=16). Mice received saline or cystamine (100 mmol in 100 μL saline) by daily intraperitoneal injection for 2 consecutive weeks. Morphological, histological, and biochemical alterations were investigated.
  
  
  RESULTS
  Cystamine decreased both left ventricular (LV) mass and LV mass/tissue-to-blood ratio (TBR) in NZB/W-F1 mice (p<0.05), whereas slight effects were observed in Balb/c mice. Moreover, cystamine reduced levels of atrial natriuretic peptide (ANP), C-reactive protein (CRP), heart type-fatty acid binding protein (h-FABP), creatine kinase-MB (CK-MB) and IL-6 in LV tissues of NZB/W-F1 mice (p<0.05). Additionally, in LV tissues of NZB/W-F1 mice, suppression of hypertrophic signaling mediated by IL-6 in response to administration of cystamine was revealed, including phosphorylation of MEK5, ERK5, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) (p<0.05).
  
  
  CONCLUSIONS
  Cystamine alleviated LV hypertrophy in NZB/W-F1 mice as a result of decrease in hypertrophic mediators and suppression of IL-6 mediated hypertrophic signaling.
authors: Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung City, Taiwan.
authors: Bor-Show
authors: BS
authors: Tzang
authors: Tsai-Ching
authors: TC
authors: Hsu
authors: Tzy-Yen
authors: TY
authors: Chen
authors: Chih-Yang
authors: CY
authors: Huang
authors: Sin-Lun
authors: SL
authors: Li
authors: Shao-Hsuan
authors: SH
authors: Kao
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D003538:Cystamine / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors; D006352:Heart Ventricles / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D015850:Interleukin-6 / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D048671:MAP Kinase Kinase 5 / Q000276:immunology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D008814:Mice, Inbred NZB; D048054:Mitogen-Activated Protein Kinase 7 / Q000276:immunology; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases / Q000037:antagonists & inhibitors; D048051:p38 Mitogen-Activated Protein Kinases / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D015850:Interleukin-6; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D048054:Mitogen-Activated Protein Kinase 7; D048051:p38 Mitogen-Activated Protein Kinases; D048671:MAP Kinase Kinase 5; C578399:Map2k5 protein, mouse; D019204:GTP-Binding Proteins; D003538:Cystamine