Exploring possible mechanisms of antiviral effect of Shufeng Jiedu Capsule on viral pneumonia: A comprehensive analysis.

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作者:Cao Shan, Bao Lei, Geng Zihan, Xu Yingli, Pang Bo, Zhang Jingsheng, Zhu Qiang, Pan Jun, Wang Yaxin, Chen Mengping, Zhang Yu, Bao Yanyan, Sun Jing, Zhao Ronghua, Cui Xiaolan, Guo Shanshan
OBJECTIVE: Influenza A virus (IAV) is a major cause of respiratory tract infections. Shufeng Jiedu Capsule (SFJD) has a broad-spectrum antiviral effect, however, it is not clear whether SFJD acts by targeting the immune-inflammatory pathway. The aim of this study was to elucidate the therapeutic effect and the mechanism of antiviral action of SFJD in mice with influenza virus pneumonia. METHODS: In this study, a mouse model of influenza virus pneumonia was used to evaluate the efficacy of SFJD in the treatment of influenza virus pneumonia. Next, the potential pathways of action by which SFJD exerts its antiviral effects were analysed in conjunction with network pharmacology and and untargeted metabolomics. Finally, in vivo experimental validation was conducted through protein immunoblotting, transmission electron microscopy, and immunofluorescence experiments. RESULTS: SFJD significantly reduced lung index, lowered viral load, attenuated lung tissue lesions, modulated inflammatory metabolism in lung tissue, reduced macrophage inflammatory infiltration and protected lung epithelial cells in mice. The results of the network pharmacological analysis and metabolomics analysis suggested that SFJD might act through the Toll-like receptor 4(TLR4)/myeloid differentiation primary response protein 88(MyD88)/ TNF receptor associated factor (TRAF6)/nuclear factor kappa-B(NF-κB) signalling pathway. SFJD was able to down-regulate the expression of TLR4, MyD88, TRAF6, and NF-κB proteins in lung tissues. CONCLUSION: SFJD could effectively attenuate lung injury induced by influenza virus infection and provide a scientific basis for the protection of respiratory mucosal epithelial cells. SFJD could effectively alleviate lung injury by regulating the TLR4/MyD88/TRAF6/NF-κB signaling pathway, inhibiting the levels of TNF-α, IL-6, which may be the key mechanism for its antiviral effects.

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