N,N-dimethylsphingosine attenuates myocardial ischemia–reperfusion injury by recruiting regulatory T cells through PI3K/Akt pathway in mice

• Published in: Basic research in cardiology 2016-05, Vol.111 (3), p.32-32, Article 32
• Main Authors: Fang, Jun, Hu, Fudong, Ke, Dan, Yan, Yuanming, Liao, Zhenmei, Yuan, Xun, Wu, Lingzhen, Jiang, Qiong, Chen, Lianglong
• Format: Article
• Language: English
• Subjects: Adoptive Transfer; Animals; Cardiology; Cardiotonic Agents - pharmacology; Disease Models, Animal; Female; Flow Cytometry; Fluorescent Antibody Technique; Male; Medicine; Medicine & Public Health; Mice; Mice, Inbred C57BL; Myocardial Reperfusion Injury - immunology; Myocardial Reperfusion Injury - pathology; Original Contribution; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Real-Time Polymerase Chain Reaction; Signal Transduction - drug effects; Signal Transduction - physiology; Sphingosine - analogs & derivatives; Sphingosine - pharmacology; T-Lymphocytes, Regulatory - drug effects; T-Lymphocytes, Regulatory - immunology
• ISSN: 0300-8428; 1435-1803
• DOI: 10.1007/s00395-016-0548-3

N , N -dimethylsphingosine (DMS) has been documented to be in vitro protective against myocardial ischemia–reperfusion injury (IRI) and can recruit CD4 + CD25 + Foxp3 + regulatory T cells (Tregs), which may participate in the cardioprotection. We hypothesized that when in vivo applied after a myocardial ischemia, DMS may be cardioprotective by recruiting Tregs. Myocardial IRI was induced in C57BL/6 mice by occluding the left main coronary arteries followed by relaxation, and DMS (0.43 mg/kg) was intravenously injected 5 min after the onset of ischemia. We found that in wild-type (WT) mice, compared with the ischemia–reperfusion group, DMS reduced the infarct size (47.1 ± 8.9 vs. 33.1 ± 3.4 %, p