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The Role of GPER in Sepsis-Induced Myocardial Cell Damage and 28-Day Mortality Risk

The Role of GPER in Sepsis-Induced Myocardial Cell Damage and 28-Day Mortality Risk

作     者:Jiangfeng Tang Jiangqin Liu Jiangfeng Tang;Jiangqin Liu

作者机构:Department of Cardiology The First Affiliated Hospital Jiangxi Medical College of Nanchang University Nanchang China Department of Emergency Gaoxin Branch of The First Affiliated Hospital Jiangxi Medical College of Nanchang University Nanchang China 

出 版 物:《Yangtze Medicine》 (长江医药(英文))

年 卷 期:2024年第8卷第3期

页      面:57-71页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主  题:G Protein-Coupled Estrogen Receptor Sepsis-Induced Cardiomyopathy Inflammation and Apoptosis Sepsis (28-Day death) Mendelian Randomization 

摘      要:Purpose: The role of GPER in sepsis-induced myocardial cell injury and its potential impact on the risk of death within 28 days in sepsis. Methods: An in vitro experiment was conducted to establish a sepsis-induced myocardial cell model. H9C2 myocardial cells were treated with 10 μg/ml lipopolysaccharide (LPS) for 24 hours. The effects of different concentrations of the GPER agonist G1 (1, 3, and 10 μmol/L) on cell viability, expression of inflammatory markers, cell apoptosis, and the NF-κB pathway were evaluated. A Mendelian randomization analysis was conducted using Single Nucleotide Polymorphism (SNPs) related to the GPER gene as instrumental variables to investigate the causal relationship between the GPER gene variations and sepsis (28-day death). Results: The results indicate that the group treated with LPS showed a significant decrease in myocardial cell viability, an increase in concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), higher apoptosis rates, and increased phosphorylation levels of NF-κB p65 (p-P65/P65) and IκB-α (p-IκB-α/IκB-α) compared to the control group (P κB pathway. However, genetic evidence did not show a causal relationship between GPER gene variations and sepsis (28-day death) (P κB pathway. However, genetic evidence did not show a causal relationship between GPER gene variations and sepsis (28-day death).

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