坏死性下垂
自噬
病毒性肺炎
自然杀伤细胞
生物
甲型流感病毒
病毒学
细胞凋亡
程序性细胞死亡
免疫学
病毒
细胞毒性T细胞
医学
生物化学
体外
内科学
传染病(医学专业)
疾病
2019年冠状病毒病(COVID-19)
作者
Rong Ma,Ruiqing Ma,Bei Chen,Li-Yu Wang,Xiao‐Yong Fan
出处
期刊:Planta Medica
[Georg Thieme Verlag KG]
日期:2021-02-05
卷期号:87 (07): 538-549
被引量:3
摘要
Abstract Influenza viral infections are prone to global outbreaks and cause pneumonia in affected populations. High morbidity and mortality caused by pneumonia occur during an influenza pandemic. Antivirals or control of inflammation is the primary means of influenza treatment. A compound cocktail composed of arctiin, daidzein, glycyrrhizic acid, and liquiritin inhibited mouse pneumonia resulting from a PR8 viral infection and caused a weight gain after oral administration. Natural killer cell activating receptors, both Ly49D and Ly49H in the lungs, were increased in the treatment in mice. In H3N2 virus-infected natural killer-92MI cells, the cocktail treatment had different effects on phosphorylation sites of phospholipase Cγ1 (PLCγ1) and killed infected cells through necroptosis or late apoptosis, in which RIP3 was increased and both caspase-3 and phosphorylated-JNK in the cells were downregulated. Acid phosphatase activity in viral-infected natural killer-92MI cells was induced by the compound cocktail treatment, which could be related to the p62 decrease in natural killer-92MI cells. In addition, an autophagic flux induction was observed in alveolar basal epithelial cells (A549). Protein p65, but not phosphorylated-p65, was significantly decreased by the treatment. Our results indicate that the compound cocktail strengthened the phosphorylation of PLCγ1-related necroptosis and partial autophagy in natural killer cells, which could yield an inhibitory effect on viral pneumonia in influenza.
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