Thirty-two male low-density lipoprotein receptor gene knockout（LDLR^－/－） mice were randomly divided into control group， model group， Sal B group， and atorvastatin group，and there were 8 mice in each group. Except for control group （fed with ordinary feed）， the mice in the other groups were fed with high-fat feed for 12 weeks.The mice in control group and model group were injected intraperitoneally with normal saline daily， the mice in Sal B group were injected intraperitoneally with Sal B solution， and the mice in atorvastatin group were administered with atorvastatin solution by gavage. The serum levels of total cholesterol（TC）， triglyceride（TG），and low density lipoprotein-cholesterol（LDL-c）of the mice in various groups were detected. Oil red O staining method was used to observe the percentages of aortic atherosclerotic plaque area of the mice in various groups. The RAW 264.7 cells were divided into control group，ox-LDL induction group （induced by 40 mg·L^－1 ox-LDL for 24 h）， low， middle， and high doses of Sal B groups（given 1.25， 2.50，and 5.00 mg·L^－1 Sal B）. Real-time fluorescence quantitative PCR（RT-qPCR）and Western blotting methods were used to detect the expression levels of AXL， MERTK， TYRO3，and milk fat globule epidermal growth factor 8（MFGE8）mRNA and proteins in arterial tissue of the mice and RAW264.7 cells in various groups.

Compared with control group， the serum levels of TC， TG， and LDL-C of the mice in model group were increased （P<0.01）， and the percentage of aortic atherosclerotic plaque area was increased （P<0.01），the expression levels of AXL， MERTK， TYRO3， and MFGE8 mRNA and proteins in arterial tissue were significantly decreased（P<0.05 or P<0.01）. Compared with model group， the serum levels of TC， TG， LDL-C of the mice in Sal B and atorvastatin groups were decreased （P<0.01）， and the percentages of aortic atherosclerotic plaque areas were decreased （P<0.01）； the expression levels of AXL， MERTK， TYRO3 and MFGE8 mRNA and proteins in arterial tissue of the mice were increased （P<0.05 or P<0.01）. Compared with control group， the expression levels of AXL， MERTK， TYRO3， MFGE8 mRNA and proteins in the RAW264.7 cells in ox-LDL group were decreased （P<0.05）； compared with ox-LDL induction group， the expression levels of AXL， MERTK， TYRO3，and MFGE8 mRNA and proteins in the RAW264.7 cells in Sal B groups were increased （P<0.05 or P<0.01）.

Sal B promotes the efferocytosis of the LDLR^－/－ mice and RAW264.7 cells by up-regulating the expressions of efferocytosis-related molecules， thereby exerting an anti-atherosclerotic effect.