Abstract: CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases. CD36 was recently found to be widely expressed in various cell types in the nervous system, including endothelial cells, pericytes, astrocytes, and microglia. CD36 mediates a number of regulatory processes, such as endothelial dysfunction, oxidative stress, mitochondrial dysfunction, and inflammatory responses, which are involved in many central nervous system diseases, such as stroke, Alzheimer’s disease, Parkinson’s disease, and spinal cord injury. CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand, thereby achieving inhibition of CD36-mediated pathways or functions. Here, we reviewed the mechanisms of action of CD36 antagonists, such as Salvianolic acid B, tanshinone IIA, curcumin, sulfosuccinimidyl oleate, antioxidants, and small-molecule compounds. Moreover, we predicted the structures of binding sites between CD36 and antagonists. These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.

Key words: animal experiments, antagonists, CD36 antagonist, central nervous system diseases, clinical trial, curcumin, microRNA, salvianolic acid B, small-molecule drugs, sulfosuccinimidyl oleate