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Liraglutide attenuate central nervous inflammation and demyelination through AMPK and pyroptosis‐related NLRP3 pathway
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Liraglutide attenuate central nervous inflammation and demyelination through AMPK and pyroptosis‐related NLRP3 pathway
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Journal Article
Liraglutide attenuate central nervous inflammation and demyelination through AMPK and pyroptosis‐related NLRP3 pathway
2022
Overview
Aims
Multiple sclerosis (MS) still maintains increasing prevalence and poor prognosis, while glucagon‐like peptide‐1 receptor (GLP‐1R) agonists show excellent neuroprotective capacities recently. Thus, we aim to evaluate whether the GLP‐1R agonist liraglutide (Lira) could ameliorate central nervous system demyelination and inflammation.
Methods
The therapeutic effect of Lira was tested on experimental autoimmune encephalitis (EAE) in vivo and a microglia cell line BV2 in vitro.
Results
Lira administration could ameliorate the disease score of EAE mice, delay the disease onset, ameliorate pathological demyelination and inflammation score in lumbar spinal cord, reduce pathogenic T helper cell transcription in spleen, restore phosphorylated adenosine monophosphate‐activated protein kinase (pAMPK) level, autophagy level, and inhibit pyroptosis‐related NLR family, pyrin domain‐containing protein 3 (NLRP3) pathway in lumbar spinal cord. Additionally, cell viability test, lactate dehydrogenase release test, and dead/live cell staining test for BV2 cells showed Lira could not salvage BV2 from nigericin‐induced pyroptosis significantly.
Conclusion
Lira has anti‐inflammation and anti‐demyelination effect on EAE mice, and the protective effect of Lira in the EAE model may be related to regulation of pAMPK pathway, autophagy, and NLRP3 pathway. However, Lira treatment cannot significantly inhibit pyroptosis of BV2 cells in vitro. Our study provides Lira as a potential candidate for Multiple Sclerosis treatment.
Liraglutide (Lira) has neuroprotective effect on experimental autoimmune encephalitis (EAE) mice, and the protective effect of Lira in the EAE model may be related to regulation of pAMPK level, autophagy, and NLRP3 pathway. However, Lira treatment cannot significantly inhibit pyroptosis of BV2 cells in vitro.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Agonists
/ AMP
/ AMP-Activated Protein Kinases
/ AMPK
/ Animals
/ Demyelinating Diseases - drug therapy
/ Experimental allergic encephalomyelitis
/ experimental autoimmune encephalitis
/ Glucagon
/ Glucose
/ Insulin
/ Kinases
/ Liraglutide - therapeutic use
/ Mice
/ NLPR3
/ NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
/ Original
/ Proteins
/ Spleen
