{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:56:54Z","timestamp":1787317014340,"version":"build-2736575974"},"reference-count":38,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2020,3,29]],"date-time":"2020-03-29T00:00:00Z","timestamp":1585440000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100011002","name":"National Natural Science Foundation of China-Yunnan Joint Fund","doi-asserted-by":"publisher","award":["81670770"],"award-info":[{"award-number":["81670770"]}],"id":[{"id":"10.13039\/501100011002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2018A0303130297"],"award-info":[{"award-number":["2018A0303130297"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2018A030313535"],"award-info":[{"award-number":["2018A030313535"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims\/Introduction<\/jats:title>\n                    <jats:p>Diabetic hearts are more vulnerable to ischemia\u2010reperfusion injury (I\/RI). The activation of nucleotide\u2010binding oligomerization domain\u2010like receptor protein\u00a03 (NLRP3) inflammasome can mediate the inflammatory process, and hence might contribute to myocardial I\/RI. Activation of autophagy can eliminate excess reactive oxygen species and alleviate myocardial I\/RI in diabetes. The present study aimed to investigate whether the activation of autophagy can alleviate diabetic myocardial I\/RI through inhibition of NLRP3 inflammasome activation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>A dose of 65\u00a0mg\/kg streptozotocin was given by tail vein injection to establish a type\u00a01 diabetes model in the rats. The left anterior descending coronary artery was ligated for 30\u00a0min followed by reperfusion for 2\u00a0h to establish a myocardial I\/RI model. H9C2 cardiomyocytes were exposed to high glucose (33 mmol\/L) and subjected to hypoxia\u2013reoxygenation (6\u00a0h hypoxia followed by 4\u00a0h reoxygenation).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The diabetic rats showed significant inhibition of cardiac autophagy (decreased LC3\u2010II\/I and increased p62) that was concomitant with increased activation of NLRP3 inflammasome (increased NLRP3, apoptosis\u2010related spots protein cleaved caspase\u20101, interleukin\u201018, interleukin\u20101\u03b2) and more severe myocardial I\/RI (elevated creatine kinase myocardial band, lactate dehydrogenase and larger infarct size). However, administration of rapamycin, an inhibitor of the autophagy, to activate autophagy resulted in the inhibition of NLRP3 inflammasome, and finally alleviated myocardial I\/RI.\n                      <jats:italic>In\u00a0vitro<\/jats:italic>\n                      , high glucose inhibited autophagy, while activating NLRP3 inflammasome in H9C2 cardiomyocytes and aggravating hypoxia\u2013reoxygenation injury, but rapamycin reversed these adverse effects of high glucose.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Activation of autophagy can suppress the formation of NLRP3 inflammasome, which in turn attenuates myocardial ischemia\u2010reperfusion injury in diabetic rats.<\/jats:p>\n                  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