Amelioratory effect of neoandrographolide on myocardial ischemic‐reperfusion injury by its anti‐inflammatory and anti‐apoptotic activities
| Autor: | Hong-li Zhang, Fei Ye, Ying Liu, Yan-fang Zhao, Xiao-Rui Yin, Yun Liu, Fen-Fang Yu, Xiang-Qi Wu |
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| Rok vydání: | 2021 |
| Předmět: |
Male
Tetrahydronaphthalenes medicine.drug_class Health Toxicology and Mutagenesis Anti-Inflammatory Agents Apoptosis Myocardial Reperfusion Injury Management Monitoring Policy and Law Pharmacology Toxicology Anti-inflammatory Proinflammatory cytokine Mice Glucosides In vivo medicine Animals Myocytes Cardiac business.industry NF-kappa B General Medicine medicine.disease In vitro Rats Cytoplasm Diterpenes Signal transduction business Reperfusion injury |
| Zdroj: | Environmental Toxicology. 36:2367-2379 |
| ISSN: | 1522-7278 1520-4081 |
| DOI: | 10.1002/tox.23350 |
| Popis: | In the present study, we aimed to evaluate the cardioprotective effect of neoandrographolide (Neo) on myocardial ischemia/reperfusion injury (I/R) models and explore its possible mechanism. We randomly and equally divided male mice into sham-operation, I/R, and I/R + Neo 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-κB 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-3, P-IKBa, and P-NF-κB protein expressions, and the translocation of NF-kB subunit p65 from the cytoplasm to the nucleus in vivo or in vitro. Still, ejected fraction, fractional shortening, and the bcl-2 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-2 and NF-κB signaling pathways. |
| Databáze: | OpenAIRE |
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