Journal of thoracic disease · 2026
Fagopyrum acutatum extract attenuates influenza A virus-stimulated inflammation and acute lung injury in vitro and in vivo.
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Liu Jinbing, Zhou Yingxuan, Huang Hanwei, Li Conglin, Ke Jiayi, Liu Lifu, Chen Yintong, Gao Taotao, Liang Xiaoli, Xu Youhua, Yang Zifeng
Аннотация
BACKGROUND: Fagopyrum acutatum is used in Chinese medicine for its heat-clearing, detoxifying and pus-expelling properties, particularly for respiratory diseases. However, the effect of Fagopyrum acutatum on inflammation induced by influenza A virus (IAV) remains unclear. This study aimed to assess how Fagopyrum acutatum extract (FAE) affected the inflammation underlying mechanisms of IAV in vitro and in vivo.
METHODS: The pharmacodynamic components in FAE were identified using ultrahigh-performance-liquid-chromatography (UPLC)-Q-Exactive mass spectrometry (MS). The mechanism of FAE was predicted through RNA sequencing (RNA-seq) analysis and confirmed via reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. The protective effects of FAE on lung injury and systemic inflammation were evaluated based on survival rate, lung index, histopathological alterations in lung tissues, lung cytokine levels, leukocyte counts in peripheral blood and serum inflammatory factor levels.
RESULTS: There were 103 compounds (mainly carbohydrates and organic acids) identified in FAE. FAE reversed the IAV-induced expression of RIG-I, MDA5, TLR3, IP-10, IL-6, IL-8, IL-1β, TNF-α, and MCP-1 in A549 cells, and reduced NF-κB P65 and IKBα phosphorylation. In vivo, FAE improved survival rates, decreased lung index and alleviated pathological changes in lung tissue caused by IAV. Expression of MCP-1, TNF-α, IL-6, IP-10 in lung tissues of mice with influenza pneumonia decreased by FAE. In addition, FAE significantly improved H1N1-induced leukocyte alterations and serum cytokine levels.
CONCLUSIONS: FAE effectively alleviates IAV-stimulated inflammation and lung damage via NF-κB signaling pathway.
METHODS: The pharmacodynamic components in FAE were identified using ultrahigh-performance-liquid-chromatography (UPLC)-Q-Exactive mass spectrometry (MS). The mechanism of FAE was predicted through RNA sequencing (RNA-seq) analysis and confirmed via reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. The protective effects of FAE on lung injury and systemic inflammation were evaluated based on survival rate, lung index, histopathological alterations in lung tissues, lung cytokine levels, leukocyte counts in peripheral blood and serum inflammatory factor levels.
RESULTS: There were 103 compounds (mainly carbohydrates and organic acids) identified in FAE. FAE reversed the IAV-induced expression of RIG-I, MDA5, TLR3, IP-10, IL-6, IL-8, IL-1β, TNF-α, and MCP-1 in A549 cells, and reduced NF-κB P65 and IKBα phosphorylation. In vivo, FAE improved survival rates, decreased lung index and alleviated pathological changes in lung tissue caused by IAV. Expression of MCP-1, TNF-α, IL-6, IP-10 in lung tissues of mice with influenza pneumonia decreased by FAE. In addition, FAE significantly improved H1N1-induced leukocyte alterations and serum cytokine levels.
CONCLUSIONS: FAE effectively alleviates IAV-stimulated inflammation and lung damage via NF-κB signaling pathway.