Melatonin protects sheep endometrial epithelial cells against lipopolysaccharide-induced inflammation in vitro.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
melatonin | decrease | expression of inflammatory factors | LPS-stimulated sheep endometrial epithelial cells | concentration-response manner | attenuated | #1 |
melatonin | decrease | LPS-stimulated phosphorylation of ERK1/2, JNK and NF-κB p65 | LPS-stimulated sheep endometrial epithelial cells | - | inhibited | #2 |
luzindole | no change | attenuation of inflammatory factors expression by melatonin | LPS-stimulated sheep endometrial epithelial cells | - | partially blocked | #3 |
4P-PDOT | no change | attenuation of inflammatory factors expression by melatonin | LPS-stimulated sheep endometrial epithelial cells | - | partially blocked | #4 |
LY294002 | no change | inhibition of LPS-induced inflammation by melatonin | LPS-stimulated sheep endometrial epithelial cells | - | abolished | #5 |
melatonin | decrease | LPS-induced endometrial epithelial cell inflammation | sheep | - | had an inhibitory effect | #6 |
Melatonin has known anti-inflammatory effects. Yet, how melatonin protects sheep endometrial epithelial cells from inflammation remains unknown. In this study, we investigated the melatonin synthetase AANAT and HIOMT and melatonin membrane receptors MT1 and MT2 distribution in sheep uterus. Using lipopolysaccharide (LPS)-stimulated sheep endometrial epithelial cells as an in vitro inflammation model. The results showed that melatonin attenuated the expression of inflammatory factors in a concentration-response manner. Melatonin also inhibited the LPS-stimulated phosphorylation of ERK1/2, JNK and NF-κB p65. This attenuation was partially blocked by luzindole (a non-specific MT1 and MT2 inhibitor) or 4P-PDOT (specific MT2 inhibitor). In addition, the above inhibition of melatonin was abolished by the PI3K/AKT pathway inhibitor LY294002. It was concluded that melatonin had an inhibitory effect on LPS-induced endometrial epithelial cell inflammation in sheep, which was mediated by the activation of the PI3K/AKT pathway via melatonin receptors.