Protective effects and regulatory mechanisms of melatonin in a neonatal mouse model of LPS-induced inflammation.

This experiment mainly explored the protective effect and regulatory mechanism of melatonin (MEL) through its receptor on central nervous system (CNS) inflammation induced by lipopolysaccharide (LPS). The experiment was first divided into the following four groups: control group (CTRL group), LPS-induced inflammation model group (LPS group), LPS-treated MEL group (LPS + MEL group), and MEL administration group (MEL group). Later, a luzindole-antagonized LPS-MEL cotreatment group (LPS + MEL + LUZ group) was added to clarify the experimental results. ELISA was used to determine the inflammatory factor levels IL-6, IL-1β, and IL-10 in brain slices. Western blotting was used to determine the expression levels of the microglia-specific protein CD11b and melatonin receptors MT1 and MT2 in brain slices. A large amount of IL-6 release and increased expression of CD11b protein were detected 24 h after inflammatory stimulation, while pretreatment with MEL inhibited the release of IL-6 and increased the expression of CD11b. At the same time, LPS induction downregulated the relative protein expression levels of MT1 and MT2. In addition, compared with the CTRL group and the LPS + MEL group, the administration of LUZ inhibited the protein expression of MT1. It increased the release of IL-1β and IL-10, further indicating that MEL can alleviate LPS-induced neuroinflammation through the MT1 response. In short, MEL can reduce the neuroinflammatory response induced by LPS and exhibit related protective effects through MT1.