Zhang Lian-Qing, Zheng Wen-Can, Li Wen-Yan
Department of Pharmacy, Shanghai Changhai Hospital, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Department of Pharmacy, First People's Hospital of Qujing City, Yunnan, China.
J Inflamm Res. 2025 Mar 17;18:3901-3911. doi: 10.2147/JIR.S466737. eCollection 2025.
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.
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.
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.
Zhike Erfang can alleviate pneumonia caused by MRSA by inhibiting TRAF6 and inducing NLRP3 inflammatory body activation.
止嗽二方在调节与耐甲氧西林金黄色葡萄球菌（MRSA）诱导的急性肺损伤相关的细胞反应和免疫微环境方面的治疗效果尚不清楚。本研究旨在阐明止嗽二方在实验室模型中减轻MRSA细胞和分子效应的潜在机制。
使用热灭活的MRSA建立急性肺损伤小鼠模型。收集肺组织和支气管肺泡灌洗液进行分析。巨噬细胞在暴露于热灭活的MRSA 24小时前用止嗽二方预处理30分钟。使用蛋白质印迹法定量肺组织中TRAF6、诱导型一氧化氮合酶（iNOS）、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、NLRP3和半胱天冬酶-1的蛋白表达。通过乳酸脱氢酶细胞毒性检测试剂盒检测乳酸脱氢酶（LDH）的含量。
止嗽二方以剂量依赖性方式显著降低MRSA模型肺组织中iNOS、LDH、TNF-α、IL-1β、NLRP3和半胱天冬酶-1的表达。止嗽二方抑制TRAF6的表达。
止嗽二方可通过抑制TRAF6和诱导NLRP3炎性小体活化来减轻MRSA引起的肺炎。
