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• The ethanol extract of Usnea diffracta shows a positive antiatherogenic effect. • The ethanol extract of Usnea diffracta promotes lipid metabolism. • The ethanol extract of Usnea diffracta reduces the plaque area in atherosclerotic model rats. • The mechanism may be related to the inhibition of TLR5/NF-κB signaling pathway. Usnea diff ;racta Vain. (U. diffracta) belonging to the Usnea genus, is widely used as a folk medicine for the treatment of ulcer, abdominal pain, diarrhea, malaria and so on. However, the antiatherogenic effect of U. diffracta has not yet been reported. This study aims to investigate the antiatherogenic effects of the ethanol extract of U. diffracta and its mechanism. A high fat diet and VD3 were used to establish the atherosclerotic rat model, with 0.004 g/kg/d of simvastatin as a positive control, fed with 0.7, 1.4, and 2.8 g/kg/d of Usnea ethanol extract for 21 days. The blood, liver, and aorta samples from each rat were collected after the last administration. Pharmacodynamic effects were evaluated. The inflammation related factors, the gene expressions of Toll-like receptor 5 (TLR5), myeloid differentiating factor 88 (MyD88), and nuclear factor-κB (NF-κB) were detected. Compared with the model group, simvastatin and ethanol extract of U. diffracta can significantly reduce the serum levels of triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), Ca2+, AST, ALT, the liver contents of total cholesterol (TC), TG, AI and liver index, as well as significantly increase the contents of high-density lipoprotein cholesterol (HDL-C) both in serum and liver (p < 0.01 or p < 0.05). The serum level of ox-LDL can be significantly reduced by simvastatin, low and medium U. diffracta ethanol extract doses (p < 0.01). In addition, simvastatin and low dosage of U. diffracta ethanol extract can significantly reduce the liver content of LDL-C (p < 0.01). U. diffracta ethanol extract shows a positive antiatherogenic effect. Furthermore, the mechanism may be related to promoting the expression of serum IL-10 and inhibition of TLR5/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]