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J Neuroimmunol ; 337: 577067, 2019 12 15.
Article in English | MEDLINE | ID: mdl-31629984

ABSTRACT

Curcumin has been used in the study of central nervous system immune-related diseases and exerts a substantial neuroprotective effect. However, the mechanism remains unclear. The AKT/mTOR autophagy-related signalling pathway plays an important role in tumour therapy, but whether curcumin plays a therapeutic role in multiple sclerosis (MS) through this signalling pathway remains to be determined. As an animal model of MS, experimental autoimmune encephalomyelitis (EAE) is induced by the myelin glial glycoprotein MOG35-55 in female C57BL/6 mice. We first evaluated the changes in autophagy levels in EAE mice. Then, curcumin was intraperitoneally injected into the mice, and the expression of AKT/mTOR autophagy signalling pathway-related proteins was evaluated. Our data show that 1. autophagy defects can cause neuronal damage in EAE mice; and 2. curcumin may regulate the activation of autophagy in EAE mice by affecting the AKT/mTOR autophagy signalling pathway, further balancing central nervous system and peripheral autophagy.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Autophagy/physiology , Curcumin/therapeutic use , Encephalomyelitis, Autoimmune, Experimental/drug therapy , Encephalomyelitis, Autoimmune, Experimental/metabolism , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Autophagy/drug effects , Curcumin/pharmacology , Encephalomyelitis, Autoimmune, Experimental/immunology , Female , Gene Expression , Mice , Mice, Inbred C57BL , Random Allocation
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