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Druckers team, the mechanism of anti-inflammatory action of GLP-1RAs was explored, revealing a key role for the CNS in regulating this anti-inflammatory effect.423 The study began by inducing inflammation in mice through the injection of various Toll-like receptor (TLR) agonists and then assessed the inflammation by measuring plasma tumor necrosis factor-alpha (TNF-) levels.423 It was observed that the GLP-1RA, exendin-4, significantly reduced the TNF- levels caused by various TLR agonists, indicating that exendin-4 can lower the TNF- levels induced by multiple TLR agonists.423 The research further demonstrated that this anti-inflammatory effect was not mediated by GLP-1R in the blood or endothelial cells but required the GLP-1R in the CNS
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% relative survival was normalized to shRNA controls (n = 3 technical replicates representative from 3 independent experiments)
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