Gegen Qinlian Decoction Downregulates the TLR7 Signalling Pathway to Control Influenza A Virus Infection

• Published in: Biomedicine & pharmacotherapy 2020-01, Vol.121, p.109471-109471, Article 109471
• Main Authors: Shi, Yucong, Xu, Huachong, Xiao, Yike, Liu, Pei, Pang, Peng, Wu, Sizhi, Deng, Li, Chen, Xiaoyin
• Format: Article
• Language: English
• Subjects: Gegen qinlian decoction; Influenza virus; TLR7
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2019.109471

•Gegen Qinlian decoction of influenza is mediated by the TLR7 pathway, and Gegen Qinlian decoction downregulated the expression of some key TLR7 signalling pathway factors.•Influenza viruses cause immune imbalances and Gegen Qinlian decoction also affected the differentiation of CD4+ T cells.•Gegen Qinlian decoction activated a balanced inflammatory response in the host to limit immune pathological injury and improve clinical and survival outcomes. In recent years, Gegen Qinlian decoction (GQD) has been applied to treat influenza virus infection, and its clinical effectiveness has been shown. However, the potential mechanism by which GQD acts on influenza A virus (IAV) has not been fully elucidated. Traditional Chinese medicine (TCM) formulas are well known to have multiple targets and effects. Our previous experiments examined the mechanism by which TCM can be used to treat influenza from the perspective of the influenza immune mechanism. To explore the possible mechanism by which GQD affects mice infected with the FM1 strain of influenza virus. Forty-eight C57BL/6 mice were divided randomly into four groups: a normal control (NG) group, an IAV infection (VG) group, an IAV + oseltamivir (30.44 mg/kg) treatment (VO) group, and an IAV + GQD (9.74 g/kg) treatment (VQ) group. We also grouped forty-eight Toll-like receptor 7 knockout (TLR7−/−) mice in the same manner. The pulmonary mRNA expression of TLR7, myeloid differentiation factor 88 (MyD88), and nuclear factor (NF)-κB p65 was measured by RT-qPCR, and the pulmonary protein expression of TLR7, MyD88, and NF-κB p65 was measured by western blot. The proportions of T helper (Th) 1, Th2, Th17 and regulatory T (Treg) cells were measured by flow cytometry. IAV infection led to low body weights and high viral load. Compared with those in the NG group, the mRNA expression levels of TLR7, MyD88, and NF-κB p65 in the VG group were upregulated (P