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Updated: Mar 11, 2026
Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Ginsenoside Rg1 mitigates sepsis-associated acute respiratory distress syndrome by promoting autophagy through the
Xiang Xue1, Changbao Huang2, Juan Chen3
1Department of Emergency Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Zhongshan East Road 305, 0000-000-8969-498X, Nanjing 210002, China.
Background:
Sepsis-associated acute respiratory distress syndrome (ARDS) is a severe condition characterized by high morbidity and mortality rates, necessitating effective therapeutic interventions. Ginsenoside Rg1 has been shown to ameliorate lung injury by targeting autophagy; however, the precise mechanisms involved remain to be elucidated.
Purpose:
The purpose of this research was to elucidate the therapeutic potential of ginsenoside Rg1 in mitigating ARDS by modulating autophagy and inhibiting apoptosis, inflammatory responses, and oxidative stress through the Prdx1-PTEN interaction.
Study Design:
This experimental study adopted complementary in vivo and in vitro models. For the in vivo assays, C57BL/6 mice were randomly assigned to the sham operation group, cecal ligation and puncture (CLP)-induced sepsis group, and multiple-dose ginsenoside Rg1 intervention groups. Additionally, Prdx1 knockout mice were utilized for genetic validation. In the in vitro experiments, alveolar epithelial cells stimulated with lipopolysaccharide (LPS) were treated with graded concentrations of Rg1. Meanwhile, cell models with Prdx1 overexpression and knockout were established to identify the therapeutic target of Rg1.
Methods:
The mechanistic effects of Rg1 on the Prdx1-PTEN interaction and its downstream signaling cascades were systematically investigated using an established murine model of sepsis induced by CLP, murine alveolar epithelial cells challenged with LPS, and genetically modified Prdx1 knockout mouse models. These complementary experimental systems were employed to dissect the molecular pathways mediating Rg1's therapeutic actions in sepsis-associated ARDS.
Results:
Administration of Rg1 significantly enhanced the molecular interaction between Prdx1 and PTEN, and inhibited the PI3K/AKT signaling pathway, leading to increased autophagic activity and decreased apoptosis, inflammation, and oxidative stress in both in vivo and in vitro models of sepsis-induced acute lung injury.
Conclusion:
These results underscore the potential of Rg1 as a therapeutic option for sepsis-induced ARDS by targeting the Prdx1-PTEN interaction to enhance autophagy. Future clinical investigations are needed to explore the therapeutic application of Rg1 in sepsis-associated ARDS.
