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CD36 inhibition partially attenuates myocardial injury in diabetic rats with ischemic postconditioning
  1. Yuan Zhang,
  2. Huimin Liu,
  3. Si Shi,
  4. Lili Chen,
  5. Rong Chen,
  6. Zhongyuan Xia,
  7. Qingtao Meng
  1. Department of Anaesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China
  1. Correspondence to Professor Qingtao Meng; mengqingtao2018{at}


Introduction To investigate the role of CD36 (fatty acid translocation enzyme) in the myocardial ischemia reperfusion (IR) injury in diabetes with ischemic postconditioning (IPostC).

Research design and methods Adult male Sprague-Dawley rats received streptozotocin treatment to establish type 1 diabetic model. After 8 weeks, diabetic rats were subjected to myocardial IR and IPostC with or without sulfo-N-succinimidyl oleate (SSO, an inhibitor of CD36) intervention.

Results Diabetic rats showed the upregulation of myocardial CD36 expression and the increase in free fatty acid (FA) and triglycerides (TG) level and FA β oxidation (FAO). The cardioprotection of IPostC was compromised in diabetic rats with myocardial IR as evidenced by increased myocardial infarct size and plasma levels of lactate dehydrogenase (LDH), creatine kinase MB isoenzyme (CK-MB), and cardiac troponin Ⅰ (cTn-I), but not in non-diabetic rats with myocardial IR. SSO significantly decreased the levels of plasma LDH, CK-MB, cTn-I, free FA, and the levels of myocardial malondialdehyde, 8-isoprostane, FA, TG, and CD36 expression, and significantly increased the levels of myocardial glutathione peroxidase, total glutathione/oxidized glutathione, FAO, peroxisome proliferator activated receptor alpha, pyruvate dehydrogenase kinase 4, and the early (E) and late (A) diastolic filling ratio of heart in diabetic rats with IR and IPostC. However, no significant differences were observed in myocardial infarct size, heart rate, ejection fraction, fractional shorting, and dp/dtmax.

Conclusions CD36 downregulation partially attenuated myocardial IR injury in diabetic rats with IPostC via ameliorating FA metabolism and oxidative stress.

  • CD36 antigens
  • myocardium
  • ischemia
  • diabetes mellitus, type 1

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information. Not applicable.

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Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information. Not applicable.

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  • YZ, HL, SS and LC are joint first authors.

  • YZ, HL, SS and LC contributed equally.

  • Contributors YZ and SS drafted the manuscript. HL and YZ analyzed and interpreted the work. HL and QM designed the work. SS, LC, and RC performed the experiments. QM and ZX reviewed it critically for important intellectual content. All authors contributed to the manuscript and approved the final version. MQT had full access to all the data in the study and had final responsibility for the decision to submit for publication.

  • Funding This work was supported by the National Natural Science Foundation of China (81401574 and 81801085).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.