RESUMO
Microglial cells are the resident immune cells of brain. The activated microglia produces a range of deleterious substances, which plays an important role in the inflammation of post-stroke, such as superoxide, nitric oxide, matrix metalloproteinases, etc. The activa-tion of microglia may involve triggering receptor expressed on myeloid cells-1, Toll-like receptors 4, peroxisome proliferator-activated re-ceptors, purinergic receptors, etc. Intervention targeted to microglial receptor is becoming a new strategy for ischemic stroke.
RESUMO
Autophagy plays an important role in the regulation of activation and inflammation of microglia after ischemic stroke. The interaction between autophagy of microglia and the inflammation mediated by microglia after ischemic stroke was complex and a large num-ber of molecules were involved. The receptors of microglia activation and related substances may be possible mechanism in the regulation of microglia autophagy. Autophagy inhibitors and microglia receptor targeting therapy may provide new strategies for the clinical treatment of ischemic stroke. This paper summarized the progress of microglia autophagy after ischemic stroke.