Zheng-Guang Chen1, Hui Luo2, Shou-Chuan Wang3, Jian-Ya Xu1, Jia-Xi Li4. 1. Pediatric Institution of Nanjing University of Chinese Medicine, Nanjing 210029, China; Jingsu Key Laboratory of Pediatric Respiratory Disease, Nanjing 210029, China. 2. Traditional Chinese Medicine Department of Children׳s Hospital of Zhengzhou, Zhengzhou 450000, China. 3. Pediatric Institution of Nanjing University of Chinese Medicine, Nanjing 210029, China; Jingsu Key Laboratory of Pediatric Respiratory Disease, Nanjing 210029, China. Electronic address: wscnj2014@126.com. 4. Traditional Chinese Medicine Department of Shenzhen Children׳s Hospital, Shenzhen 518000, China.
Abstract
ETHNOPHARMACOLOGICAL 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 JOL in mice infected with respiratory syncytial virus (RSV). MATERIALS AND METHODS: Mice were orally administered JOL at doses of 27.6 g kg(-1) d(-1) and 55.2 g kg(-1) d(-1) for 1, 3, or 6d after RSV challenge. The viral loads in the lung tissue were measured by real-time RT-PCR. The levels of IFN-β 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: JOL 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-β, TLR3, IRF3 (p-IRF3), and SOCS1 were significantly downregulated in RSV-infected mice treated with JOL. However, 7d after infection, JOL significantly upregulated the RSV-induced decrease in IFN-β, TLR3, and IRF3 (p-IRF3), but reduced SOCS1 expression. CONCLUSIONS: JOL ameliorated lung inflammation and inhibited virus replication significantly in RSV-infected mice. During early stage infection, the effect of JOL was improved through inhibition of the TLR3-IRF3-IFN-β signaling pathway and the expression of SOCS1, whereas during the later stage of infection, JOL upregulated the expression of key signaling molecules in the TLR3 signaling pathway and downregulated the expression of SOCS1.
ETHNOPHARMACOLOGICAL 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 JOL in mice infected with respiratory syncytial virus (RSV). MATERIALS AND METHODS:Mice were orally administered JOL at doses of 27.6 g kg(-1) d(-1) and 55.2 g kg(-1) d(-1) for 1, 3, or 6d after RSV challenge. The viral loads in the lung tissue were measured by real-time RT-PCR. The levels of IFN-β 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: JOL significantly ameliorated lung inflammation in RSV-infectedmice, and significantly reduced the viral load in the lung tissues. On days 2 and 4 after infection, the mRNA and protein expression of IFN-β, TLR3, IRF3 (p-IRF3), and SOCS1 were significantly downregulated in RSV-infectedmice treated with JOL. However, 7d after infection, JOL significantly upregulated the RSV-induced decrease in IFN-β, TLR3, and IRF3 (p-IRF3), but reduced SOCS1 expression. CONCLUSIONS: JOL ameliorated lung inflammation and inhibited virus replication significantly in RSV-infectedmice. During early stage infection, the effect of JOL was improved through inhibition of the TLR3-IRF3-IFN-β signaling pathway and the expression of SOCS1, whereas during the later stage of infection, JOL upregulated the expression of key signaling molecules in the TLR3 signaling pathway and downregulated the expression of SOCS1.
Authors: Li Li Lin; Jin Jun Shan; Tong Xie; Jian Ya Xu; Cun Si Shen; Liu Qing Di; Jia Bin Chen; Shou Chuan Wang Journal: Evid Based Complement Alternat Med Date: 2016-09-04 Impact factor: 2.629