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Kidney Week

Abstract: FR-PO153

Embelin Attenuated Septic AKI by Inhibition of M1 Macrophage Polarization and NF-κB Signaling in Mice

Session Information

  • AKI: Mechanisms - II
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Tang, Qiao, North Sichuan Medical College, Nanchong, Sichuan, China
  • Li, Yi, Sichuan Academy of Medical Sciences and Sichuan People's Hospital, Chengdu, Sichuan, China
Background

Acute kidney injury (AKI) is a clinical syndrome with high morbidity and mortality. As one of the most common reasons to AKI, there is currently no effective treatment for sepsis beyond supportive care. Embelin could demonstrate hepatoprotective effect against acute liver injury and regulate hepatic macrophage activity. However, the therapeutic effect and immunomodulatory role underlying Embelin action in septic AKI is unclear.

Methods

Current study aimed to elucidate the role and mechanism of Embelin in lipopolysaccharide (LPS)-induced septic AKI involving macrophage activation. In the study, Embelin was once intraperitoneal injection given to the mice after LPS injection. Then harvested the serum and kidney sample after 24 h. To explore the immunomodulatory role of Embelin in macrophages, we further isolated murine bone marrow-derived macrophages (BMDMs) and stimulated murine BMDMs with LPS followed by Embelin treatment.

Results

We observed that Embelin attenuated renal dysfunction and renal pathological damage following LPS injection. Embelin could inhibit translocation of phosphorylated NF-κB p65 in LPS-induced AKI in vivo and vitro. Embelin also reduced the secretion of IL-1β and IL-6 whereas increased the secretion of IL-10 and Arg-1 both in BMDMs and murine serum after LPS induction.

Conclusion

It indicated that Embelin could suppress macrophage M1 activation and promote M2 polarization in LPS-induced AKI. Thus, Embelin could attenuate LPS-induced septic AKI by suppress of NF-κB p65 phosphorylation and regulated macrophage activation. This study suggested the potential therapeutic role of Embelin for septic AKI patients.