Abstract
Influenza virus H5N1 triggers “cytokine storm” related to acute lung injugry (ALI) leading to high mortality in the patients once upon the virus infection. Previous study demonstrated that hemagglutinin (HA) of H5N1 induced ALI by disturbing airway epithelial cAMP-dependent CFTR channel through activation of TLR4/JAK3. Furthermore, Tianlongkechuanling(TL), a traditional Chinese formulae, had the effects on inhibiting H5N1 HA-induced ALI. Moreover, the property could be reproduced by triple combinations of ferulic acid(F), quercetin(Q) and glycyrrhizic acid(G) which are the representative active ingredients of TL’s major compounds (flavonoids, Phenolic acids and triterpenoids),respectively. However, the specific mechanisms of FQG are unknown.
In the present study, using chamber recordings (short-circuit current), real-time PCR, Immunofluorescence and Liquidchip assay were performed through comparing the effects on anti-ALI of monomers with that of FQG in vitro and in vivo to explore FQG therapeutic mechanisms. FQG has much more better effects on countering acute lung damage induced by H5N1 HA than those of monomers. And FQG can significantly not only inhibite the actived JAK3 but also activate cAMP-dependent CFTR channel. F plays important role of the triple combanations.
All data above indicate that triple combinations of FQG as agonists for cAMP-CFTR/PKA to modulate activated JAK3 yield synergy in the treatment of acute lung injury induced by H5N1 HA.
Footnotes
Cite this article as Eur Respir J 2022; 60: Suppl. 66, 1242.
This article was presented at the 2022 ERS International Congress, in session “-”.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
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