Abstract Necroptosis is a new type of cell death. However, the role of necroptosis in LPS-related cardiomyocyte damage has not been fully understood. The aim of our study is to explore the molecular mechanism underlying inflammation-mediated cardiomyocyte necroptosis. H9C2 cardiomyocyte cell line was treated with LPS. Then, cell viability and necroptosis were measured through qPCR and ELISA. Pathway analysis was performed to verify whether Ripk3/Pgam5 signaling pathway is implicated into the regulation of cardiomyocyte necroptosis. The results demonstrated that LPS reduced cardiomyocyte viability and activated necroptosis. At the molecular levels, oxidative stress and inflammation were triggered by LPS and these alterations may contribute to the activation of necroptosis. Finally, we found that Ripk3/Pgam5 signaling pathway was activated by LPS in cardiomyocyte and this signaling pathway may explain the regulatory mechanism underlying LPS-mediated necroptosis. Altogether, our results demonstrated that septic cardiomyopathy is associated with an activation of necroptosis through the Ripk3/Pgam5 signaling pathway.

中文翻译：

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LPS 通过 Ripk3/Pgam5 信号通路诱导心肌细胞坏死

摘要 坏死性凋亡是一种新型的细胞死亡。然而，坏死性凋亡在 LPS 相关心肌细胞损伤中的作用尚未完全清楚。我们研究的目的是探索炎症介导的心肌细胞坏死的分子机制。H9C2 心肌细胞系用 LPS 处理。然后，通过 qPCR 和 ELISA 测量细胞活力和坏死性凋亡。进行通路分析以验证 Ripk3/Pgam5 信号通路是否涉及心肌细胞坏死性凋亡的调节。结果表明 LPS 降低了心肌细胞的活力并激活了坏死性凋亡。在分子水平上，氧化应激和炎症是由 LPS 引发的，这些改变可能有助于激活坏死性凋亡。最后，我们发现 Ripk3/Pgam5 信号通路在心肌细胞中被 LPS 激活，该信号通路可能解释了 LPS 介导的坏死性凋亡的调控机制。总之，我们的结果表明，脓毒性心肌病与通过 Ripk3/Pgam5 信号通路激活坏死性凋亡有关。