Antiviral effects of Jinxin oral liquid against respiratory syncytial virus infection in the BALB/c mice model

作者 Chen, Zheng-Guang; Luo, Hui; Wang, Shou-Chuan; Xu, Jian-Ya; Li, Jia-Xi

期刊 JOURNAL OF ETHNOPHARMACOLOGY , MAR 13 2015,:162

DOI 10.1016/j.jep.2015.01.002 PubMed 25593018

摘要 Ethnopharrnacological relevance: Jinxin oral liquid (JOL) is used in traditional Chinese medicine (TCM) to treat influenza, cough, asthma, and viral pneumonia, on the basis of Ma Xing Shi Gan Tang (MXSGT) and the clinical experience of Professor Wang Shouchuan, one of the most prestigious pediatricians in China.Aim of study: To investigate the anti-inflammatory and antiviral activities of JUL in mice infected with respiratory syncytial virus (RSV).Materials and methods: Mice were orally administered JUL at doses of 27.6 g kg(-1) d(-1) and 55.2 g kg(-1) d(-1) for 1, 3, or 6 d after RSV challenge. The viral loads in the lung tissue were measured by real-time RT-PCR. The levels of IFN-beta in bronchoalveolar lavage fluid (BLAF) and lung tissue were detected by ELISA and real-time RT-PCR, respectively. The mRNA and protein expression of TLR3, IRF3, and SOCS1 were detected by real-time RT-PCR and western blot, respectively. The protein expression of phoshorylated-IRF3 (p-IRF3) was detected by western blot.Results: JUL significantly ameliorated lung inflammation in RSV-infected mice, and significantly reduced the viral load in the lung tissues. On days 2 and 4 after infection, the mRNA and protein expression of IFN-beta, TLR3, IRF3 (p-IRF3), and SOCS1 were significantly downregulated in RSV-infected mice treated with JUL However, 7 d after infection, JUL significantly upregulated the RSV-induced decrease in IFN-beta, TLR3, and IRF3 (p-IRF3), but reduced SOCS1 expression.Conclusions: JUL ameliorated lung inflammation and inhibited virus replication significantly in RSV-infected mice. During early stage infection, the effect of JUL was improved through inhibition of the TLR3-IRF3-IFN-13 signaling pathway and the expression of SOCS1, whereas during the later stage of infection, JUL upregulated the expression of key signaling molecules in the TLR3 signaling pathway and downregulated the expression of SOCS1. (C) 2015 Elsevier Ireland Ltd. All rights reserved.