Analysis of the neuroprotective effect of GLP‐1 receptor agonist peptide on cerebral ischemia‐reperfusion injury by Quantitative Proteomics Mass Spectrometry

Abstract

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.

Abstract

Liraglutide, a GLP‐1 receptor agonist, effectively reduced the infarct volume in the brain in MCAO mice. The physiological effects of liraglutide in ischemia‐reperfusion injury were dependent on the suppression of oxidative stress, on the inhibition of neuronal apoptosis and a reduction in the inflammatory response.