TNF and acute respiratory distress syndrome: XBJ targets significant molecules, such as ACE2 and AKT1, blocking viral cell entry, replication, and dissemination, thus manifesting its antiviral properties.[22] Additionally, XBJ is capable of reducing the levels of inflammatory mediators, including IL-2, IL-4, and TNF-α, and influences various signaling pathways, including PI3K-AKT, NF-κB, MAPK, and Toll-like receptors.[23] XBJ may offer a therapeutic benefit for acute respiratory distress syndrome through the modulation of immune cell/cytokine pathways and mitigation of cytokine storms.