文献类型： 外文期刊

作者： Jing, Junsong ³ ; Sun, Yi ³ ; Shui, Yiyang ³ ; Wang, Junyi ² ; Ye, Wenjing ² ; Chen, Ranran ³ ; Wu, Lianhao ³ ; Xing, Lijuan ³ ; Huang, Rongrong ³ ; Zhou, Ting ² ; Zhu, Wenwen ² ; Wu, Yueguo ² ; Zhang, Sheng ⁴ ; Shi, Jing ² ; Li, Yuanyuan ² ; Liu, Yan ¹ ; You, Zhenqiang ⁴ ;

作者机构： 1.Hangzhou Med Coll, Sch Basic Med & Forens, Hangzhou, Peoples R China

2.Zhejiang Acad Agr Sci, Inst Sericulture & Tea, Hangzhou, Peoples R China

3.Hangzhou Med Coll, Sch Pharmaceut Sci, Hangzhou, Peoples R China

4.Hangzhou Med Coll, Sch Publ Hlth, 182 Tianmushan Rd, Hangzhou 310013, Zhejiang, Peoples R China

5.Hangzhou Med Coll, Ctr Safety Evaluat & Res, Hangzhou, Peoples R China

6.Hangzhou Med Coll, Key Discipline Zhejiang Prov Publ Hlth & Prevent M, Class 1,Category A, Hangzhou, Peoples R China

关键词： Influenza viral pneumonia; C -type signaling receptor pathway; Dectin-1/Syk; Network pharmacology; Morus alba L.

期刊名称：PHYTOMEDICINE （ 影响因子：8.3； 五年影响因子：8.0 ）

ISSN： 0944-7113

年卷期： 2025 年 140 卷

页码：

收录情况： SCI

摘要： Background: Viral pneumonia is an infection of the lungs caused by numerous different viruses, which can lead to severe respiratory distress and even life-threatening conditions. In the absence of specific treatments for viral pneumonia, natural traditional medicines offer an alternative in terms of innovative drug therapies. Morus alba L. (common name mulberry leaf) is a Chinese medicine that has been used clinically as an antiviral. Purpose: The therapeutic effect of M. alba on viral pneumonia was investigated along with its mechanism of action. Methods: Network pharmacology and molecular docking were used to analyze the mechanism of action of M. alba in the treatment of viral pneumonia. Histology, immunofluorescence, Western blotting, qPCR, and flow cytometry were used to evaluate the protective effect of MLE (the ethanol extract of Morus alba L.) on PR8 (A/ Puerto Rico/8/1934 H1N1, a murine lung-adapted influenza A virus strain)-induced viral pneumonia. SiRNA was used to validate the relationship between the therapeutic effects of MLE on viral pneumonia and the target Syk (a crucial non-receptor tyrosine kinase). Results: MLE alleviated PR8-induced viral pneumonia by reducing inflammatory factor expression in the lungs, decreasing NF-kappa B pathway activation, slowing oxidative damage in the lungs, and inhibiting lung tissue cell apoptosis. Meanwhile, MLE for viral pneumonia was significantly associated with Syk targets. Notably, knockdown of the Syk gene not only reduced the therapeutic effect of MLE, but also suppressed PR8-induced viral pneumonia. Conclusion: MLE can alleviate PR8-induced viral pneumonia through inhibiting the Dectin-1/Syk pathway.