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

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