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Molecules. 2019 Nov 20;24(23). pii: E4219. doi: 10.3390/molecules24234219. [h=1]Effect of Forsythiaside A on the RLRs Signaling Pathway in the Lungs of Mice Infected with the Influenza A Virus FM1 Strain.[/h]
Zheng X[SUP]1[/SUP], Fu Y[SUP]1[/SUP], Shi SS[SUP]1[/SUP], Wu S[SUP]1[/SUP], Yan Y[SUP]1[/SUP], Xu L[SUP]1[/SUP], Wang Y[SUP]1[/SUP], Jiang Z[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology and Immunology, Basic Medicine College, Jinan University, GuangZhou 510632, China. 2 Institute of Medical Microbiology, Jinan University, GuangZhou 510632, China.
[h=3]Abstract[/h] Forsythiaside A, a phenylethanoid glycoside monomer extracted from Forsythia suspensa, shows anti-inflammatory, anti-infective, anti-oxidative, and antiviral pharmacological effects. The precise mechanism underlying the antiviral action of forsythiaside A is not completely clear. Therefore, in this study, we aimed to determine whether the anti-influenza action of forsythiaside A occurs via the retinoic acid-inducible gene-I-like receptors (RLRs) signaling pathway in the lung immune cells. Forsythiaside A was used to treat C57BL/6J mice and MAVS[SUP]-/-[/SUP] mice infected with mouse-adapted influenza A virus FM1 (H1N1, A/FM1/1/47 strain), and the physical parameters (body weight and lung index) and the expression of key factors in the RLRs/NF-κB signaling pathway were evaluated. At the same time, the level of virus replication and the ratio of Th1/Th2 and Th17/Treg of T cell subsets were measured. Compared with the untreated group, the weight loss in the forsythiaside A group in the C57BL/6J mice decreased, and the histopathological sections showed less inflammatory damage after the infection with the influenza A virus FM1 strain. The gene and protein expression of retinoic acid-inducible gene-I (RIG-I), MAVS, and NF-κB were significantly decreased in the forsythiaside A group. Flow cytometry showed that Th1/Th2 and Th17/Treg differentiated into Th2 cells and Treg cells, respectively, after treatment with forsythiaside A. In conclusion, forsythiaside A reduces the inflammatory response caused by influenza A virus FM1 strain in mouse lungs by affecting the RLRs signaling pathway in the mouse lung immune cells.
[h=4]KEYWORDS:[/h] A/FM1/1/47 strain); MAVS−/− mice; RLRs signaling pathway; forsythiaside A; influenza A virus FM1 mouse lung adaptive strain (H1N1
PMID: 31757053 DOI: 10.3390/molecules24234219
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Zheng X[SUP]1[/SUP], Fu Y[SUP]1[/SUP], Shi SS[SUP]1[/SUP], Wu S[SUP]1[/SUP], Yan Y[SUP]1[/SUP], Xu L[SUP]1[/SUP], Wang Y[SUP]1[/SUP], Jiang Z[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology and Immunology, Basic Medicine College, Jinan University, GuangZhou 510632, China. 2 Institute of Medical Microbiology, Jinan University, GuangZhou 510632, China.
[h=3]Abstract[/h] Forsythiaside A, a phenylethanoid glycoside monomer extracted from Forsythia suspensa, shows anti-inflammatory, anti-infective, anti-oxidative, and antiviral pharmacological effects. The precise mechanism underlying the antiviral action of forsythiaside A is not completely clear. Therefore, in this study, we aimed to determine whether the anti-influenza action of forsythiaside A occurs via the retinoic acid-inducible gene-I-like receptors (RLRs) signaling pathway in the lung immune cells. Forsythiaside A was used to treat C57BL/6J mice and MAVS[SUP]-/-[/SUP] mice infected with mouse-adapted influenza A virus FM1 (H1N1, A/FM1/1/47 strain), and the physical parameters (body weight and lung index) and the expression of key factors in the RLRs/NF-κB signaling pathway were evaluated. At the same time, the level of virus replication and the ratio of Th1/Th2 and Th17/Treg of T cell subsets were measured. Compared with the untreated group, the weight loss in the forsythiaside A group in the C57BL/6J mice decreased, and the histopathological sections showed less inflammatory damage after the infection with the influenza A virus FM1 strain. The gene and protein expression of retinoic acid-inducible gene-I (RIG-I), MAVS, and NF-κB were significantly decreased in the forsythiaside A group. Flow cytometry showed that Th1/Th2 and Th17/Treg differentiated into Th2 cells and Treg cells, respectively, after treatment with forsythiaside A. In conclusion, forsythiaside A reduces the inflammatory response caused by influenza A virus FM1 strain in mouse lungs by affecting the RLRs signaling pathway in the mouse lung immune cells.
[h=4]KEYWORDS:[/h] A/FM1/1/47 strain); MAVS−/− mice; RLRs signaling pathway; forsythiaside A; influenza A virus FM1 mouse lung adaptive strain (H1N1
PMID: 31757053 DOI: 10.3390/molecules24234219
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