Reply to “Loganin: A potential pharmacological agent for myocardial ischemia-reperfusion injury”

Our recent work published in the International Journal of Cardiology suggests that loganin treatment inhibits oxidative stress and cellular apoptosis in myocardial ischemia-reperfusion injury (MIRI) in part via Janus kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) [ [1] Xia B. Ding J. Li Q. Zheng K. Wu J. Huang C. et al. Loganin protects against myocardial ischemia-reperfusion injury by modulating oxidative stress and cellular apoptosis via activation of JAK2/STAT3 signaling. Int. J. Cardiol. 2023; 131426 Google Scholar ]. We greatly appreciate the comments of Li et al. suggesting that the anti-inflammatory property of loganin may also explain its protective effect against MIRI. We agree with this view, because our follow-up experiments showed that loganin significantly altered the expression of interleukin-10 (IL-10) in the ischemic area of the left ventricle in mice that received an ischemia-reperfusion stimulus. However, because IL-10 functions as an anti-inflammatory cytokine with immunosuppressive functions, further studies are needed to determine the specific role of IL-10 signaling and to evaluate whether differences in other inflammatory factors are involved in loganin-mediated cardioprotection.