Objective: The pathological characteristics of cerebral ischemia-reperfusion injury (CIRI) are complex, and the mechanism involved remains unknown. The treatment for CIRI has become an increasingly important challenge in the clinic, prompting us to explore the mechanism of CIRI. It was reported that GLP-1 receptor agonist, Liraglutide, exhibited alleviating effects on CIRI. The previous findings suggested that the administration of Liraglutide in rodents results in the attenuation of the infarct volume following ischemia-reperfusion injury by mediating the reactive oxygen species, apoptotic and necroptotic pathways.
Methods: Here, a proteomic study was performed aiming to clarify the physiological protection role of GLP-1 receptor agonist during the development of CIRI in MCAO mice. This proteomic investigations is contributed to reveal the mechanism associated with the treatment of GLP-1 receptor agonist in MCAO mice.
Results: The results indicated that the occurrence of ischemia-reperfusion led to complex pathological processes, including inflammation, necroptosis and apoptosis. The treatment of Liraglutide significantly reduced the infract volume resulted from ischemia reperfusion injury. The proteomic data revealed that the administration of Liraglutide in MCAO mice induced the various effects on proteins expression level and phosphorylation.
Conclusions: The findings in this study was beneficial for identifying the novel therapeutic target for the treatment of ischemia reperfusion.
Keywords: cerebral ischemia reperfusion injury; proteomics.
© 2021 The Authors. Brain and Behavior published by Wiley Periodicals LLC.