Lian-Qing Zhang,1,* Wen-Can Zheng,2 Wen-Yan Li3,* 

1Department of Pharmacy, Shanghai Changhai Hospital, The First Affiliated Hospital of Naval Medical University, Shanghai, China; 2Department of Pharmacy, First People’s Hospital of Qujing City, Yunnan, China; 3Department of Clinical Pharmacy, Gongli Hospital of Shanghai Pudong New Area, Shanghai, China

*These authors contributed equally to this work

Correspondence: Wen-Yan Li, Department of Clinical Pharmacy, Gongli Hospital of Shanghai Pudong New Area, Shanghai, People’s Republic of China, Tel/Fax +86-021-58858730-5296, Email liwenyan_linda@163.com

Purpose: The therapeutic effects of Zhike Erfang in modulating the cellular responses and immune microenvironment associated with MRSA-induced acute lung injury remain unclear. This study aims to elucidate the potential mechanisms by which Zhike Erfang mitigate the cellular and molecular effects of MRSA in a laboratory model.
Patients and Methods: A mouse model of acute lung injury was established using heat-inactivated MRSA. Lung tissue and bronchoalveolar lavage fluid were collected for analysis. Macrophages were pretreated with Zhike Erfang for 30 minutes before exposure to heat-inactivated MRSA for 24 hours. Protein expressions of TRAF6, iNOS, TNF-α, IL-1β, NLRP3, and caspase-1 in lung tissues were quantified using Western blot. The content of LDH was detected by the lactate dehydrogenase cytotoxicity test kit.
Results: Zhike Erfang significantly reduced the expression of iNOS, LDH, TNF-α, IL-1β, NLRP3, and caspase-1 in a dose-dependent manner in lung tissues from the MRSA model. Zhike Erfang inhibited the expression of TRAF6.
Conclusion: Zhike Erfang can alleviate pneumonia caused by MRSA by inhibiting TRAF6 and inducing NLRP3 inflammatory body activation.

Keywords: Zhike Erfang, methicillin-resistant Staphylococcus aureus, TRAF6, NLRP3, pneumonia