Open Access

ARTICLE

Glycyrrhizic acid alleviates lung injury in sepsis through SIRT1/HMGB1 pathway

by BINGJIE LIN¹, XIAOBO YING², CHUANLING ZHANG^3,*, GUOJUN ZHANG^1,*

1 Infectious Diseases Department, The First People’s Hospital of Fuyang Hangzhou, Hangzhou, 311400, China
2 Infectious Diseases Department, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, 311201, China
3 Translational Medicine Laboratory, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, 311201, China

* Corresponding Authors: CHUANLING ZHANG. Email: ; GUOJUN ZHANG. Email:

BIOCELL 2024, 48(11), 1613-1623. https://doi.org/10.32604/biocell.2024.053652

Received 07 May 2024; Accepted 09 August 2024; Issue published 07 November 2024

Abstract

Objectives: This study explores the protective effects of glycyrrhizic acid (GA) on sepsis-induced cellular damage and inflammation in acute lung injury (ALI), specifically through the modulation of the sirtuin 1 (SIRT1) and high mobility group box 1 (HMGB1) pathway. Methods: The study employed two experimental models: lipopolysaccharide (LPS)-induced BEAS-2B human lung epithelial cells and cecal ligation and puncture (CLP) rats, to simulate sepsis conditions. The cell model involved treatments with LPS, GA, control siRNA (si-NC), and SIRT1-specific siRNA (si-SIRT1). Evaluations included cell viability, apoptosis, and cytokine production. In the rat model, treatments included GA and the SIRT1 inhibitor EX527, with assessments on lung tissue damage, inflammation, and protein expression using Western blot and co-immunoprecipitation (Co-IP) analysis. Results: LPS exposure significantly reduced SIRT1 mRNA levels and cell viability in BEAS-2B cells, which effects were reversed by co-treatment with GA and si-NC but negated by si-SIRT1. LPS also induced apoptosis and increased pro-inflammatory cytokines and HMGB1 expression, which were mitigated by GA and si-NC and exacerbated by si-SIRT1. In CLP rats, GA treatment decreased lung tissue damage, inflammatory cytokines, and HMGB1 expression, and enhanced SIRT1 levels. However, these protective effects were reversed when GA was combined with EX527. Conclusion: GA demonstrates significant protective effects against LPS-induced damage and inflammation in lung cells and tissue by modulating the SIRT1-HMGB1 pathway. This suggests that GA could be a potential therapeutic strategy for treating sepsis and related inflammatory conditions.

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Keywords

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