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,n5）. On the contrary, the adiponectin protein was decreased（P<0.05,n5）. 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,n5）. The adiponectin level in the cell supernatant was decreased （at 15 pmol/L most obvious） （P<0.05,n5 ）, while level of the MCP-1 went down without statistically significant difference （P>0.05,n5）. 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,n5） in a dose-dependent manner. The secretion of MCP-1 and adiponectin did not change significantly in 3T3-L1 adipocytes （P>0.05,n5）. 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.