GLP-1R agonist liraglutide attenuates pain hypersensitivity by stimulating IL-10 release in a nitroglycerin-induced chronic migraine mouse model

Glucagon-like peptide-1 receptor (GLP-1R) has been indicated to involve in chronic pain, however, the mechanism by which GLP-1R alleviates the central sensitization of chronic migraine (CM) remains unclear. Treatment with GLP-1R agonist liraglutide attenuated trigeminal allodynia and suppressed the protein levels of CMassociated molecules in the trigeminal nucleus caudalis (TNC). Further analysis showed that injection of liraglutide stimulated the release of IL-10 in the TNC. Treatment with IL-10 also alleviated pain hyperalgesia. Our findings illustrated that liraglutide might alleviate the central sensitization of CM by stimulating the release of IL10, which reveals a novel mechanism of CM.

Automated summary

Glucagon-like peptide-1 receptor (GLP-1R) is involved in chronic pain, but the mechanism by which GLP-1R alleviates central sensitization of chronic migraine (CM) is unclear. Treatment with GLP-1R agonist liraglutide reduced trigeminal allodynia and decreased CM-associated molecules in the trigeminal nucleus caudalis (TNC). Further analysis showed that liraglutide injection stimulated the release of IL-10 in the TNC, and IL-10 treatment also alleviated pain hyperalgesia. Our findings suggest that liraglutide may alleviate CM central sensitization by stimulating IL-10 release, revealing a novel mechanism.