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文献引用产品|小鼠肌酸激酶同工酶MB(CK-MB)ELISA试剂盒

发布人:上海雅吉生物科技有限公司

发布日期:2026/5/12 8:53:21

 文章标题:Amelioratory effect of neoandrographolide on myocardial ischemic-reperfusion injury by its anti-inflammatory and anti-apoptotic activities

影响因子:4.119
期刊:ENVIRONMENTAL TOXICOLOGY
作者列表:Ying Liu, Yun Liu, Hong-Li Zhang, Fen-Fang Yu, Xiao-Rui Yin, Yan-Fang Zhao, Fei Ye, Xiang-Qi Wu
发表时间:2021-8-16
DOI:10.1002/tox.23350
主要研究成果:Abstract
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.


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