Huashibaidu formula attenuates sepsis-induced acute lung injury via suppressing cytokine storm: Implications for treatment of COVID-19

Phytomedicine. 2023 Jan:109:154549. doi: 10.1016/j.phymed.2022.154549. Epub 2022 Nov 19.

Abstract

Background: Acute lung injury (ALI) is a common complication of sepsis with poor effective interventions. Huashibaidu formula (HSBD) showed good therapeutic effects in treating coronavirus disease 2019 (COVID-19) patients.

Purpose: This study was designed to investigate the therapeutic potential and precise mechanism of HSBD against sepsis-induced ALI based on network pharmacology and animal experiments.

Materials and methods: Network pharmacology was used to predict the possible mechanism of HSBD against sepsis. Next, a sepsis-induced ALI rat model via intraperitoneal lipopolysaccharide (LPS) was constructed to evaluate the level of inflammatory cytokines and the degree of lung injury. The expression of inflammation-related signaling pathways, including TLR4/NF-κB and PI3K/Akt was determined by western blot.

Results: Network pharmacology analysis indicated that HSBD might have a therapeutic effect on sepsis mainly by affecting inflammatory and immune responses. Animal experiments demonstrated that HSBD protected the lung tissue from LPS-induced injury, and inhibited the levels of inflammatory cytokines such as interleukin (IL)-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN)-γ and tumor necrosis factor (TNF)-α in the serum and IL-1β, IL-5, IL-6, IL-18, GM-CSF, IFN-γ and TNF-α in the lung tissue. Western blot results revealed that HSBD downregulated the expression of TLR4/NF-κB and upregulated the expression of PI3K/Akt.

Conclusion: The therapeutic mechanism of HSBD against sepsis-induced ALI mainly involved suppressing cytokine storms and relieving inflammatory symptoms by regulating the expression of TLR4/NF-κB and PI3K/Akt. Our study provides a scientific basis for the mechanistic investigation and clinical application of HSBD in the treatment of sepsis and COVID-19.

Keywords: Acute lung injury; COVID-19; Cytokine storm; Huashibaidu formula; Lipopolysaccharide; Sepsis.

MeSH terms

  • Acute Lung Injury* / drug therapy
  • Acute Lung Injury* / etiology
  • Animals
  • COVID-19
  • Cytokine Release Syndrome* / drug therapy
  • Cytokine Release Syndrome* / virology
  • Cytokines / metabolism
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Sepsis* / complications
  • Sepsis* / drug therapy
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • NF-kappa B
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha