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Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury

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Abstract

Currently, treatment options for acute lung injury (ALI) are limited. Gypenoside XLIX (Gyp-XLIX) is known for its anti-inflammatory properties, but there is a lack of extensive research on its effects against ALI. This study induced ALI in mice through cecal ligation and puncture surgery and investigated the biological activity and potential mechanisms of Gypenoside XLIX (40 mg/kg) by intraperitoneal injection. The in vitro ALI model was established using mouse lung epithelial (MLE-12) cells stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Various methods, including Hematoxylin and Eosin (H&E) staining, biochemical assay kits, Quantitative Polymerase Chain Reaction (qPCR) analysis, Western blotting, Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) assay, immunofluorescence, and flow cytometry, were employed for this research. The results indicated that pretreatment with Gypenoside XLIX significantly alleviated pathological damage in mouse lung tissues and reduced the expression levels of inflammatory factors. Additionally, Gypenoside XLIX inhibited ROS levels and NLRP3 inflammasome, possibly mediated by the Sirt1/Nrf2 signaling pathway. Moreover, Gypenoside XLIX significantly inhibited sepsis-induced lung cell apoptosis and excessive autophagy of mitochondria. Specifically, it suppressed mitochondrial pathway apoptosis and the Pink1/Parkin pathway of mitochondrial autophagy. These findings reveal the multifaceted effects of Gypenoside XLIX in anti-inflammatory, antioxidative, and inhibition of cell apoptosis and autophagy. This provides strong support for its therapeutic potential in sepsis-related lung injuries.

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Funding

This study was supported by grants from the Lianyungang City Science and Technology Plan Project (No. JCYJ2309), the Science Foundation of Kangda College of Nanjing Medical University (No. KD2023KYJJ052) and the Priority Academic Program Development of Jiangsu Higher Education Institutions of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Author notes

  1. Kaixin Ping, Rongrong Yang and Huizhen Chen contributed equally to this study.

Authors and Affiliations

  1. Jiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-Industry Technology, Jiangsu Marine Pharmaceutical Resources Development Engineering Research Center, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang, 222005, China

    Kaixin Ping, Shaocheng Xie, Yannan Xiang, Mengxin Li & Jingquan Dong

  2. Department of Oncology, The Second People’s Hospital of Lianyungang (The Oncology Hospital of Lianyungang), Affiliated to Kangda College of Nanjing Medical University, Lianyungang, 222000, China

    Rongrong Yang, Yannan Xiang & Yingzhi Lu

  3. Institute of Neuroscience, Neurosurgery Department, The First People’s Hospital of Lianyungang, Lianyungang, 222005, China

    Kaixin Ping, Huizhen Chen & Mengxin Li

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  1. Kaixin Ping
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Contributions

Kaixin Ping: Experiment conduction, Data curation and analysis, Methodology, Writing the original draft. Rongrong Yang: Data curation; Data analysis, Investigation, Methodology. Huizhen Chen: Investigation, Data analysis, Writing the original draft. Shaocheng Xie: Visualization, Validation, Supervision. Yannan Xiang: Software, Validation. Mengxin Li: Visualization, Investigation. Yingzhi Lu: Conceptualization, Visualization, Investigation, Supervision. Jingquan Dong: Conceptualization, Project administration, Funding acquisition, Writing review and editing.

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Correspondence to Yingzhi Lu or Jingquan Dong.

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Ping, K., Yang, R., Chen, H. et al. Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury. Inflammation (2024). https://doi.org/10.1007/s10753-024-02041-2

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