Fig. 6

The mechanic diagram of GA to protect against MDR-AB-induced cell injury. On the one hand, MDR-AB activates MYD88 by binding TLR-1, 2,4,6, and intracellular TLR-9 receptors. MYD88 activates NF-κB, and the latter trans-locates into the nucleus, resulting in the expression of inflammatory factors. On the other hand, MDR-AB can invade cells, resulting in intracellular ROS expression. Thus, excessive inflammatory cytokines and ROS accumulation eventually lead to apoptosis, while GA can reverse the trend by inhibiting inflammation and oxidative stress