Effects of Acylated Ghrelin on Monocyte Chemotactic Protein 1 and Adiponectins Parasecretion of Adipocytes Induced by Tumour-Necrosis Factor-α

Aim To investigate whether acylated ghrelin can protect 3T3-L1 mouse adipocytes from inflammatory injury mediated by inflammatoral factor tumour-necrosis factor-α( TNF-α). Methods Four experimental groups were set up: control group,TNF-α treated group,acylated ghrelin treated group and a group pretreated by acylated ghrelin followed by TNF-α treatment. After the completion of the intervention,the mRNA and protein levels of Toll-like recepter 4( TLR-4),nuclear factor κB p65( NF-κB p65) protein phosphorylation level,the concentration of monocyte chemotactic protein 1( MCP-1) and adiponectin in the supernatant were detected. Results 1 Compared with control group,mRNA and protein expression level of TLR-4 were increased by TNF-α intervention,as well as level of NF-κB p65 protein phosphorylation and MCP-1 protein in the murine 3T3-L1 adipocytes( P 0. 05,n = 5). On the contrary,the adiponectin protein was decreased( P 0. 05,n = 5). 2Compared with control group,the level of TLR-4 mRNA and protein expression,as well as NF-κB p65 protein phosphorylation were significantly decreased in acylated ghrelin treated group( P 0. 05,n = 5). The adiponectin level in the cell supernatant was decreased( at 15 pmol / L most obvious)( P 0. 05,n =5),while level of the MCP-1 went down without statistically significant difference( P 0. 05,n = 5). 3Compared with TNF-α( 100 μg / L) treated group,the incubation of acylated ghrelin could antagonise TNF-α-induced activation of TLR-4 /NF-κB pathway in mouse 3T3-L1 adipocytes,mRNA and protein expression levels of TLR-4,the level of NF-κB p65 protein phosphorylation were decreased( P 0. 05,n = 5) in a dose-dependent manner. The secretion of MCP-1 and adiponectin did not change significantly in 3T3-L1 adipocytes( P 0. 05,n = 5). Conclusions TNF-α can activate TLR-4 / NF-κB inflammatory pathways and increase secretion of pro-inflammatory cytokines( MCP-1),while decrease the secretion of anti-inflammatory cytokines( adiponectin) in 3T3-L1 adipocytes. Acylated ghrelin can antagonise TNF-α-induced activation of TLR-4 / NF-κB pathway in a dose-dependent manner in mouse 3T3-L1 adipocytes,but can not completely improve the secretion disorder of MCP-1 and adiponectin.