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. 2020 Mar 29;11(5):1126–1136. doi: 10.1111/jdi.13235

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© 2020 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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The (a) myocardial infarct size, (b) lactate dehydrogenase (LDH) and (c) creatine kinase myocardial band (CK‐MB) release in diabetic rats (DM) after ischemia‐reperfusion injury (I/RI) were significantly higher than those in non‐diabetic rats (Ctrl). Compared with the non‐diabetic group, the diabetic group had significant inhibition of autophagy, shown as (d,e) decreased LC3‐II/I and (d,f) increased p62, and activation of NLRP3 inflammasome, (g) shown as increased nucleotide‐binding oligomerization domain‐like receptor protein 3 (NLRP3), (h) apoptosis‐related spots protein (ASC), (i) caspase‐1 p20, (k) interleukin (IL)‐1β and (l) IL‐18, in the myocardium. Also, the diabetic group had more severe myocardial I/RI (elevated creatine kinase myocardial band, LDH and larger infarct size). Data are shown as the mean ± standard error of the mean. *P < 0.05 versus Ctrl sham; ^# P < 0.05 versus DM sham I/RI; and ^& P < 0.05 versus Ctrl I/RI; n = 6/group.