The molecular mechanisms behind the gastroprotective effect of the AMHAE on ethanol-induced gastric ulcers in a rat model included a decline of inflammatory process (infiltration of inflammatory cells and oedema formation), reduction of MCP-1, MDA, NF-κB, and TNF-α levels, increases of antioxidants (SOD, CAT, GSH-px), and upregulation of IL-4, HSP-70, NO, and PGE2 expressions. This evidence concerns the gene CCL2 and gastric ulcer.