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.

中文翻译：

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新穿心莲内酯通过抗炎和抗凋亡活性改善心肌缺血再灌注损伤的作用

在本研究中，我们旨在评估新穿心莲内酯 (Neo) 对心肌缺血/再灌注损伤 (I/R) 模型的心脏保护作用，并探讨其可能的机制。我们将雄性小鼠随机均等地分为假手术组、I/R 组和 I/R + Neo 组。H9C2 细胞系和原代新生大鼠心肌细胞被诱导进入模拟 I/R 状态，并用于进一步验证 Neo 在体外的作用。Neo治疗后在体内或体外分析心脏收缩功能、心肌损伤指标(IMI)、梗死面积、病理变化、细胞凋亡、炎性细胞因子以及与凋亡和NF-κB信号通路相关的指标。与 I/R 组相比，Neo 显着抑制 IMI、梗死面积、炎症细胞浸润、细胞凋亡、炎症细胞因子、bax、在体内或体外切割 caspase-3、P-IKBa 和 P-NF-κB 蛋白表达，以及 NF-kB 亚基 p65 从细胞质到细胞核的易位。尽管如此，在 Neo 治疗后，射血分数、缩短分数和 bcl-2 蛋白表达显着增加。Neo可通过抑制心肌炎症和细胞凋亡而开发成为治疗心肌I/R的新药，这与抑制bax/bcl-2和NF-κB信号通路的激活密切相关。