Glycyrrhetinic acid protects against Multidrug-resistant Acinetobacter baumannii-induced lung epithelial cells injury by regulating inflammation and oxidative stress

BMC Pharmacology and Toxicology

Research

Daojun Yu¹  Yida Bao²  Jing Chen²  Haitong Wan²  Yu He²  Huifen Zhou²  Liang Jin²  Jiehong Yang²  Piaoyi Guo² 

[1] Affiliated Hangzhou First People’s Hospital, Zhejiang University of Medicine, 310003, Hangzhou, Zhejiang, PR China;Zhejiang Chinese Medical University, 310053, Zhejiang, Hangzhou, PR China;

关键词: Multidrug-resistant Acinetobacter baumannii;    Glycyrrhetinic acid;    Meropenem;    Cell infection;    Inflammation;    Antioxidant;   

DOI  :  10.1186/s40360-023-00648-z

 received in 2022-09-07, accepted in 2023-01-25,  发布年份 2023

来源: Springer

【 摘 要 】

Glycyrrhetinic acid (GA) is a bio-effective component of Licorice. The GA is a monomer and the ingredient is an Oleanane-type pentacyclic triterpenes that has been used as a remedy for years. Due to the abuse of antibiotics, people pay attention to the emergence of Multidrug-resistant Acinetobacter baumannii (MDR-AB). As a conditional pathogen, MDR-AB causes severe infection, endangering human lives. Our previous studies found GA played an important role in Yinhua Pinggan, a Chinese medicine. However, whether GA could protect lung epithelium from MDR-AB-induced cell injury was elusive. Herein, we investigated the effects of GA on MDR-AB-infected A549 cells. The results showed GA had slightly antibacterial activity to MDR-AB in the GA (high concentration) but no impact on drug resistance genes. Notwithstanding, GA could reverse MDR-AB-induced cell apoptosis, hampered adhesion and invasion of MDR-AB to cells, and inhibit pro-inflammatory cytokines expression of IL-1β, IL-6, and TNF. Besides, MDR-AB-induced reactive oxygen species, pro-oxidative protein malonaldehyde, and myeloperoxidase of cells were decreased by GA, while antioxidative proteins were recovered, showing antioxidative capacity of GA might play a critical role. The expressions of toll-like receptor (TLRs) - 1, 2, 4, 5, 6, and 9 were increased by MDR-AB infection, while GA reversed the tendency. Interestingly, GA inhibited MDR-AB induced myeloiddifferentiationfactor88 expression (MYD88), one downstream con-factors of TLRs, but no affection on Interferon regulatory Factor 3 (IRF3), the other one, indicating GA inhibited MDR-AB induced cell injury by impact TLR/MYD88 pathway to attenuate inflammation. Altogether, our results demonstrated that GA protects against MDR-AB-induced cell injury through its antioxidative and anti-inflammatory properties, which deserve further study in the future.

【 授权许可】

CC BY   
© The Author(s) 2023

【 图 表 】

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