Lei Biao, Huang Wenbo, Peng Wei, Mu Jingwen, Liu Yi, Zhou Chunxian, Cheng Ting, Wei Xiaojiao, Pan Lingyun, Zheng Yuejuan, Fang Bangjiang
Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
The Research Center for Traditional Chinese Medicine, Shanghai Institute of Infectious Diseases and Biosecurity, School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Infect Drug Resist. 2025 Jul 31;18:3829-3846. doi: 10.2147/IDR.S499548. eCollection 2025.
Shu-Feng-Jie-Biao formula (SFJBF) has been used to treat acute respiratory infections for a dozen years. This study aimed to explore its mechanisms and effects for the treatment of influenza.
Network pharmacology was used to explore the underlying mechanism of SFJBF against influenza. The protective effects of SFJBF in vivo were evaluated by lung indexes, body weight loss and pathological changes in lungs. The anti-inflammatory effects in vivo were evaluated by flow cytometry and ELISA. RAW264.7 cells stimulated with imiquimod (R837) were used to determine the anti-inflammatory effects of SFJBF. Neutrophils isolated from bone marrow were activated by phorbol 12-myristate 13-acetate (PMA) to validate the effects of the active components of SFJBF.
SFJBF protected body weight loss, decreased lung indexes, reduced total protein content in lungs and mitigated pathological changes in mice. SFJBF inhibited the expression of chemokines ( and ) and cytokines ( and IL-6) accompanied by the decreased infiltration of neutrophils in lungs. SFJBF inhibited the expression of iNOS and MPO in lungs. The synergistic role of OSV and SFJBF was exhibited by suppressing virus-induced cytokine expression and reducing the infiltration of inflammatory monocytes in lungs. SFJBF inhibited the phosphorylation of ERK1/2 and NF-κBp65, thereby reducing the secretion of MIP-2, TNF-α, MCP-1 and CCL5 in vitro The active components of SFJBF, including baicalin and wogonin, reduced the production of reactive oxygen species (ROS), MIP-2, MCP-1, and IL-6 in vitro.
SFJBF ameliorated virus-induced lung injury by suppressing overactivated immune responses via NF-κB and ERK MAPK signaling pathways, thereby protecting mice from influenza virus infection. SFJBF could be considered a potent therapeutic agent for treating influenza.
疏风解表方已用于治疗急性呼吸道感染十余年。本研究旨在探讨其治疗流感的机制和效果。
采用网络药理学方法探讨疏风解表方抗流感的潜在机制。通过肺指数、体重减轻和肺组织病理变化评估疏风解表方在体内的保护作用。采用流式细胞术和酶联免疫吸附测定法评估其在体内的抗炎作用。用咪喹莫特（R837）刺激RAW264.7细胞以确定疏风解表方的抗炎作用。从骨髓中分离的中性粒细胞用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）激活，以验证疏风解表方活性成分的作用。
疏风解表方可减轻体重减轻，降低肺指数，减少肺组织总蛋白含量，减轻小鼠肺组织病理变化。疏风解表方抑制趋化因子（和）和细胞因子（和白细胞介素-6）的表达，同时减少肺组织中性粒细胞浸润。疏风解表方抑制肺组织中诱导型一氧化氮合酶（iNOS）和髓过氧化物酶（MPO）的表达。通过抑制病毒诱导的细胞因子表达和减少肺组织炎性单核细胞浸润，显示出氧化苦参碱（OSV）与疏风解表方的协同作用。疏风解表方抑制细胞外信号调节激酶1/2（ERK1/2）和核因子κB p65（NF-κBp65）的磷酸化，从而减少体外巨噬细胞炎症蛋白-2（MIP-2）、肿瘤坏死因子-α（TNF-α）、单核细胞趋化蛋白-1（MCP-1）和C-C基序趋化因子5（CCL5）的分泌。疏风解表方的活性成分，包括黄芩苷和汉黄芩素，在体外减少活性氧（ROS）、MIP-2、MCP-1和白细胞介素-6的产生。
疏风解表方可通过NF-κB和ERK丝裂原活化蛋白激酶（MAPK）信号通路抑制过度激活的免疫反应，改善病毒诱导的肺损伤，从而保护小鼠免受流感病毒感染。疏风解表方可被认为是治疗流感的有效治疗剂。
