Progress of Pharmacological Research on XBJI
Modern pharmacological studies have shown that XBJI is anti-inflammatory, antioxidant, immune-regulatory, and protects against acute lung injury (see  Table 3 ).
Tiantian Li et al. found that in mice with MRSA-induced sepsis, XBJI protected the infected mice by downregulating expression of inflammatory cytokines stimulated by Pam3CSK4, MAPK, PI3K (phosphatidylinositol 3 kinase)/Akt and other pathways, thus, inhibiting the inflammatory response (Li T. T. et al., 2020). Shuwen Zhang et al. and Xi Chen et al. found that XBJI significantly reduced TNF-α, IL-6, and IL-10 levels in mice with sepsis, prevented neutrophil infiltration of lung and kidney, modulated T helper cell (Th) 1/Th2, Th17, and Tregs balance, reduced inflammatory response, and improved survival rate in mice with infectious shock (Zhang et al., 2006; Chen et al., 2018). Mingwei Liu et al. studied rats with paraquat-induced acute lung injury and discovered that XBJI could enhance immunity, reduce expression of inflammatory factors, and protect against acute lung injury by blocking p-38 MAPK and NF-κB p65 pathways, (Liu et al., 2014). Research by Yin Teng et al. found that XBJI in combination with conventional treatment significantly reduced interleukin-1 (IL-1), IL-6, and TNF-α levels, improved CD4+/CD8+ T lymphocyte ratio and NK cell relative activity, reduced inflammatory response, and enhanced cellular immunity in patients with severe pneumonia (Teng et al., 2012). Research by Hui Jin et al. showed that XBJI significantly improved the activity of superoxide dismutase (SOD), reduced reactive oxygen species (ROS) levels and protected against oxidative damage in mice under high-temperature stimulation (Jin et al., 2018). Research by Luo Peng et al. showed that XBJI downregulated MDA levels, upregulated SOD levels, and alleviated LPS-induced acute lung injury in rats (Luo and Zhou, 2017). In a rat model of oleic acid or LPS-induced acute lung injury, XBJI reduced TNF-α levels, alleviated pulmonary tissue edema and inflammatory cell infiltration, and protected against lung injury (Zhang et al., 2014). Research by Yuexia Ma et al. showed that although XBJI had no direct antiviral effect in mice with H1N1 severe pneumonia; it alleviated lung injury and protected against death, which might be due to its regulation of inflammatory cytokine levels in the early stage (Ma et al., 2015).