Stellate Ganglion Block Attenuates LPS-Induced Acute Lung Injury by Activating Sirt3 Regulation of Oxidative Stress

Shiyun Dai1,2, Jun Ji3, Rongrong Li1

  • 1Department of Anesthesiology, Second Affiliated Hospital of Naval Medical University, Shanghai 200003, China.

Biomedicines
|June 27, 2024
PubMed

Insights

Stellate ganglion blocks (SGB) can reduce lung injury by activating Sirt3 signaling. This process helps regulate oxidative stress and inflammation, offering a new protective strategy for acute lung injury (ALI).

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Cellular Signaling

Background:

  • Stellate ganglion blocks (SGBs) are used for pain but their role in acute lung injury (ALI) is unclear.
  • Previous studies suggest SGBs may attenuate ALI in animal models, necessitating further mechanistic investigation.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which SGBs attenuate lipopolysaccharide (LPS)-induced ALI in rats.
  • To investigate the role of Sirt3 signaling in mediating the protective effects of SGBs against ALI.

Main Methods:

  • Rats were divided into control, saline, LPS, and LPS + SGB groups.
  • Evaluated lung tissue damage, blood gases, macrophage differentiation, inflammatory cytokines (IL-1β, IL-6, IL-10), oxidative stress markers (ROS, CYP-D, T-SOD, Mn-SOD, CAT), and Sirt3 signaling pathway proteins (JAK2/STAT3, NF-κb p65, CIRP, NLRP3).

Main Results:

  • SGB treatment attenuated lung damage, improved oxygenation, and promoted M2 macrophage differentiation.
  • SGB reduced pro-inflammatory cytokines (IL-1β, IL-6) and increased anti-inflammatory IL-10.
  • SGB inhibited oxidative stress (ROS, CYP-D) and enhanced antioxidant enzyme activity (T-SOD, Mn-SOD, CAT).
  • SGB upregulated Sirt3 and downregulated JAK2/STAT3, NF-κb p65, CIRP, and NLRP3 signaling.

Conclusions:

  • SGB attenuates LPS-induced ALI by activating Sirt3-mediated regulation of oxidative stress and inflammation.
  • SGB represents a potential prophylactic strategy for LPS-induced ALI.