Progress of Pharmacological Research on SFJDC
Modern pharmacological studies have found that SFJDC has antiviral, antibacterial, and anti-inflammatory properties and protects against lung injury (see  Table 3 ).
Yanyan Bao et al. evaluated the broad-spectrum antiviral activity of SFJDC by cytopathic effect (CPE) inhibition. A total of eight viruses, including H1N1, herpes simplex (HSV), respiratory syncytial virus, adenovirus (ADV) and Coxsackie virus, were evaluated. SFJDC had significant in vitro broad-spectrum antiviral activity and the best inhibitory effect was against parainfluenza virus (PIV). Similar results were obtained from in vivo experiments (Qiu et al., 2014; Bao et al., 2019). Ying Liu et al. used H1N1 FM1 and PR8 strains to induce nasal drip infection in an immunocompromised mouse pneumonia model. Therapeutic and preventive effects of SFJDC were observed against H1N1 infection in vivo. The results showed that SFJDC influenced the immune function of the mice, improved pneumonia symptoms caused by influenza virus, reduced the lung index of mice infected with H1N1, significantly reduced mortality, and had good therapeutic efficacy (Liu et al., 2010). Research by Weiwei Lv et al. found that SFJDC had inhibitory activity against multiple viruses and bacteria. Its antiviral activity was inferior to that of Ribavirin, but its cytotoxicity was lower. Both antiviral activity and antibacterial action were superior to those of Qingkailing granules (QKLG) (Lv et al., 2013). Li Ma et al. used a mouse pneumonia model induced by Streptococcus pneumoniae to study the anti-inflammatory mechanism of SFJDC. They discovered that it reduced white blood cell (WBC) count, reduced serum levels of the transcription factor nuclear factor kappa B (NF-κB), MCP-1, inflammatory mediator BK and COX-2, thus, having a therapeutic effect in the model (Ma et al., 2018). Further studies found that SFJDC had a significant immune regulatory function, reducing levels of B lymphocytes, CD8+ cells, interleukin-1α (IL-1α), IL-1β, IL-2, IgM, and IgG to improve lung function in mice with pneumonia. SFJDC increased the CD4+/CD8+ ratio and number of natural killer (NK) cells, thus, having a therapeutic effect in the pneumonia model (Ma et al., 2019a; Ma et al., 2019b). Zhengang Tao et al. observed a protective function of SFJDC against endotoxin LPS-induced rat lung injury. Their results showed that SFJDC inhibited the LPS-induced inflammatory response, and reduced LPS-induced lung injury. Its mechanism of action might be inhibition of the MAPK (mitogen-activated protein kinase)/NF-κB signaling pathway and downregulation of NF-κB mRNA expression (Tao et al., 2014). Yanmei Li et al. used a Pseudomonas aeruginosa (PAK)-induced KM mouse acute lung injury model to explore the mode of action of SFJDC in treatment of acute lung injury. They found that SFJDC significantly alleviated lung injury in the model and its mode of action might be related to the ERK signaling pathway (Li et al., 2017).