Progress of mitochondrial and endoplasmic reticulum-associated signaling and its regulation of chronic liver disease by Chinese medicine

Figure 4 Molecular mechanism of Chinese medicines regulating the treatment of chronic liver disease. Silymarin increases the expression of superoxide dismutase (SOD) to reduce the levels of reactive oxygen species (ROS) and TNF-α, IL-6, IL-8, etc. to stabilize the endoplasmic reticulum (ER). Rhein is capable of anti-lipid peroxidation and scavenging of ROS, and inhibits the activities of TNF-a and IL-1β to stabilize the ER. vA significantly reduces malondialdehyde and elevates the levels of SOD to reduce ROS in mitochondria. vA has the ability to reduce lipid accumulation in hepatocytes and protect ER and Ca²⁺ homeostasis. quercetin inhibits alcohol and Ca²⁺ homeostasis through the regulation of PERK-MAMs pathway. VA has the ability to reduce intracellular lipid accumulation in hepatocytes and effectively protect ER and Ca²⁺ homeostasis. quercetin inhibits alcohol-induced iron death in hepatocytes and alleviates alcoholic liver injury through the regulation of the PERK-MAMs pathway. Composite glycyrrhizin tablets inhibit NF-κB pro-inflammatory signaling and IL-6 and IL-1β activities by inhibiting NF-κB pro-inflammatory signaling and IL-6 and IL-1β activities. transduction and IL-6 and IL-8 expression to inhibit hepatic injury, and also by promoting SOD and GSH expression as well as inhibiting malondialdehyde synthesis, induced hepatocellular injury. GSH passages inhibit ROS generation and attenuate hepatic injury caused by oxidative stress. ROS: Reactive oxygen species; ERS: Endoplasmic reticulum stress; SOD: Superoxide dismutase.