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Research Snapshot Theater: Veterinarian

The Role of Lp-PLA2 in Regulating Macrophage Inflammatory Response in Sepsis-Induced Cardiomyopathy

Sunday, March 22, 2026
2:30 PM - 3:30 PM Central Time
Location: Connections Central - RST 12
  • WX

    Wen Xu, N/A

    CHN

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • ZQ

    Zhaoxin Qian, n/a

    MD, PhD
    Xiangya Hospital Central South University

    Disclosure information not submitted.

  • ZZ

    Zhihong Zuo, n/a

    Assistant Researcher
    Critical Care Medicine,Xiangya Hospital,Central South University,Changsha,China

    Disclosure information not submitted.

Introduction: Sepsis-induced cardiomyopathy (SICM) is a transient myocardial injury induced by sepsis, with a high mortality rate and a lack of effective treatment strategies and early warning biomarkers. Lipoprotein associated phospholipase A2 (Lp-PLA2) is considered to be associated with the regulation of inflammatory responses and is an independent risk factor for many inflammation-related diseases, mainly secreted by macrophages, which are key cells in maintaining the inflammatory homeostasis of the heart. However, the role of Lp-PLA2 and macrophages in SICM is not yet clear.


Methods: This study utilized cecal ligation and puncture surgery or intraperitoneal injection of LPS to establish a mouse model of Sepsis-induced cardiomyopathy (SICM), and used LPS stimulation of macrophages to establish a cell model of SICM. Through both animal and cell levels, the specific drug Darapladib were used, combined with experimental techniques such as RT-PCR, Western blot, co-culture of cells, immunofluorescence staining, cardiac ultrasound, and ELISA, to validate the important role of Lp-PLA2 in driving macrophage inflammation in the occurrence and development of SICM.


Results: 1、 In the cardiac tissues of LPS/CLP-induced SICM mice, Lp-PLA2 expression is upregulated and primarily localized in macrophages.
2、 Darapladib downregulates the expression of inflammatory factors iNOS, Il-1β, Tnf-α, Il-6, and Il-10 in the cardiac tissues of SICM mice by inhibiting Lp-PLA2 expression and activity, and the intervention effect of 50mg/kg Darapladib is significant.
3、 A dose of 50mg/kg Darapladib significantly reduces the mortality and the expression of cardiac injury markers ANP, BNP, CK-MB, and cTnI in SICM mice, and maintains normal EF and FS values at various time points.
4、 Inhibiting Lp-PLA2 can downregulate the expression of macrophage activation markers CD68 and inflammatory factors Tnf-α, Il-6 in LPS-treated macrophages, and alleviate the damage of the supernatant from LPS-treated macrophages to the viability of H9C2 myocardial cells.


Conclusions: Lp-PLA2 regulates macrophage inflammatory response contributing to the occurrence and development of SICM. Inhibiting Lp-PLA2 may improve the prognosis of SICM, and Darapladib could potentially become a therapeutic drug for SICM patients.