Xijiao Dihuang Decoction Protects Against Murine Sepsis-Induced Cardiac Inflammation and Apoptosis via Suppressing TLR4/NF-[kappa]B and Activating PI3K/AKT Pathway

Background: Xijiao Dihuang decoction (XJDHT), a traditional Chinese medicine, is widely used to treat patients with sepsis. However, the mechanisms underlying the effects of XJDHT on cardiac dysfunction have yet to be fully elucidated. The present study evaluated the potential utility of XJDHT in pr...

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Bibliographic Details
Published in:Journal of inflammation research 2024-02, Vol.17, p.853
Main Authors: Li, Wei, Lin, Mingrui, Li, Jiapeng, Ding, Qihang, Chen, Xiaoling, Chen, Huaiyu, Shen, Zhiqing, Zhu, Xueli
Format: Article
Language:English
Subjects:
Analysis
Apoptosis
Genes
Genomics
Heart
Infection
Inflammation
Medicine, Chinese
RNA
RNA sequencing
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Summary:Background: Xijiao Dihuang decoction (XJDHT), a traditional Chinese medicine, is widely used to treat patients with sepsis. However, the mechanisms underlying the effects of XJDHT on cardiac dysfunction have yet to be fully elucidated. The present study evaluated the potential utility of XJDHT in protecting against sepsis-induced cardiac dysfunction and myocardial injury. Methods: The mice were randomly divided into 3 groups and administered Lipopolysaccharide (LPS,10 mg/kg) or equivalent saline solution (control) and treated with XJDHT (10 g/kg/day) or saline by gavage for 72 hours. XJDHT was dissolved in 0.9% sodium chloride and administered at 200 [micro]L per mouse. Transthoracic echocardiography, RNA-seq, TUNEL assays and hematoxylin and eosin (H&E) staining of cardiac tissues were performed. Results: Treatment with XJDHT significantly enhanced myocardial function and attenuated pathological change, infiltration of inflammatory cells, levels of TNF-[alpha], IL-1[beta] and expression of TLR4 and NF-[kappa]B in mice with sepsis. RNA sequencing and Kyoto Encyclopedia of Genes and Genomes pathway analyses identified 531 differentially expressed genes and multiple enriched signaling pathways including the PI3K/AKT pathway. Further, XJDHT attenuated cardiac apoptosis and decreased Bax protein expression while increasing protein levels of Bcl-2, PI3K, and p-AKT in cardiac tissues of mice with sepsis. Conclusion: In summary, XJDHT improves cardiac function in a murine model of sepsis by attenuating cardiac inflammation and apoptosis via suppressing the TLR4/NF-[kappa]B pathway and activating the PI3K/AKT pathway. Keywords: XJDHT, sepsis, inflammation, apoptosis, TLR4/NF-[kappa]B, PI3K/AKT pathway
ISSN:1178-7031
1178-7031
DOI:10.2147/JIR.S428305