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We randomly and equally divided male mice into sham\u2010operation, I\/R, and I\/R\u2009+\u2009Neo groups. H9C2 cell line and primary neonatal rat cardiomyocytes were induced into the simulated I\/R's status and used to further validate the Neo's role in vitro. Heart systolic function, indexes of myocardial injury (IMI), infarct size, pathological change, cell apoptosis, inflammatory cytokines, and indexes related to apoptotic and NF\u2010\u03baB signaling pathways were analyzed in vivo or in vitro after the Neo treatment. Compared to the I\/R group, Neo significantly suppressed IMI, infarct size, inflammatory cell infiltration, cell apoptosis, inflammatory cytokines, bax, cleaved caspase\u20103, P\u2010IKBa, and P\u2010NF\u2010\u03baB protein expressions, and the translocation of NF\u2010kB subunit p65 from the cytoplasm to the nucleus in vivo or in vitro. Still, ejected fraction, fractional shortening, and the bcl\u20102 protein expression were notably increased after the Neo treatment. Neo could be developed into a new drug for treating myocardial I\/R by inhibiting myocardial inflammation and apoptosis, which was closely related to suppressing the activation of bax\/bcl\u20102 and NF\u2010\u03baB signaling pathways.<\/jats:p>","DOI":"10.1002\/tox.23350","type":"journal-article","created":{"date-parts":[[2021,8,16]],"date-time":"2021-08-16T11:19:54Z","timestamp":1629112794000},"page":"2367-2379","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Amelioratory effect of neoandrographolide on myocardial ischemic\u2010reperfusion injury by its anti\u2010inflammatory and anti\u2010apoptotic activities"],"prefix":"10.1002","volume":"36","author":[{"given":"Ying","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology the Eighty\u2010first Hospital of PLA Affiliated with Anhui Medical University  Nanjing 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