In vitro experiments have shown significant antiviral activity against SARS-CoV, AIV H7N9, dual H1N1/H3N2, together with inhibition of Middle East Respiratory Syndrome (MERS)-CoV activity to a certain degree (Yao et al., 2020). Yuewen Ding et al. used MTT and plaque reduction assays to show that LHQWC inhibited proliferation of multiple strains of influenza virus, and reduced virus titer and levels of inflammatory cytokines in the lungs of infected mice. The results indicated that LHQWC acted as a broad-spectrum antiviral and, in particular, regulated the immune response to viral infection (Ding et al., 2017). Qi Li et al. discovered that LHQWC not only reversed LPS-stimulated expression of macrophage chemotactic factor-1 (MCP-1) by macrophages, but also significantly improved pulmonary edema in a mouse model of acute lung injury. Inhibition of expression and secretion of MCP-1 in lung tissues of model mice was accompanied by reduced infiltration of mononuclear macrophages and reduction of inflammatory injury (Li et al., 2019). Fen Ping et al. studied the effects of LHQWC on rats with oxidative lung injury caused by fine particulate matters (PM 2.5). The results showed that LHQWC significantly reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) serum levels in rats with lung injury, increased levels of glutathione peroxidase (GSH-Px), reduced pathological damage of lung tissues, and inhibited exudation of inflammatory cells into the alveolar cavity. Together, the data indicated that LHQWC protected against oxidative stress injury in the lungs of rats (Ping et al., 2016). Wenwen Cui et al. studied the impact of LHQWC in a mouse model of acute lung injury caused by intratracheal infusion of LPS. LHQWC alleviated the inflammatory response in lung tissues by downregulating the IKK/IκB/nuclear factor (NF)-κB signaling pathway, thus, protecting mice from acute lung injury (Cui et al., 2016). Siwen Tang et al. studied the effects of LHQWC intervention on pathological lung tissue injury in mice and expression of inflammatory cytokines caused by exposure to automobile exhaust. The results showed that LHQWC reduced protein and mRNA expression of inflammatory cytokines in lung tissue by reducing blood levels of inflammatory cytokines, thus, protecting against lung tissue injury caused by automobile exhaust (Tang et al., 2015).