Mechanism of Guanxinkang ameliorating hepatic steatosis by liver efferocytosis in LDLR-/-atherosclerosis model mice
Objective The research aims to observe the effect of Guanxinkang decoction on liver steatosis in LDLR-/-atheroscle-rosis mice through liver efferocytosis.Methods Eighteen LDLR-/-mice were randomly divided into model group,Guanxinkang decoction group and atorvastatin group.After 12 weeks of high-fat diet,the model group,Guanxinkang decoction group and atorvastatin group were treated with normal saline,Guanxinkang decoction 28.66g/(kg·d)and atorvastatin suspension 5 mg/(kg·d)by gavage for 12 weeks,respectively.Another six C57BL/6J mice were used as the normal control group,and were fed with normal diet for 24 weeks.The levels of serum Aspartate Aminotransferase(ALT),Aspartate Transaminase(AST),total choles-terol(TC)and Triglyceride(TG)were detected by automatic biochemical analyzer;HE and oil red O staining was used to ob-serve the pathological changes of aortic sinus and liver tissue.RT-qPCR and Western blot were used to detect liver Sphingosine-1-phosphate Receptor 1(S1P1)and Chemokine C-X3-C-Motif receptor 1(CX3CR1),MER proto-oncogene tyrosine ki-nase(MERTK)and Recombinant Milk Fat Globule EGF Factor 8(MFGE8)mRNA and protein relative expression.Re-sults Compared with the control group,the serum levels of ALT,AST,TC,and TG in the model group were significantly in-creased(P＜0.01),and pathological changes and steatosis were observed in the liver tissue.The relative expressions of S1P1,CX3CR1,MERTK,and MFGE8mRNA and protein in the liver were significantly decreased(P＜0.01).Compared with the model group,the serum levels of ALT,AST,TC and TG in the Guanxinkang decoction group were significantly decreased(P＜0.01),the pathological changes and steatosis of liver tissue were improved,and the relative expressions of S1P1,CX3CR1,MERTK and MFGE8mRNA and protein were significantly increased(P＜0.01).Conclusion Guanxinkang decoction may im-prove liver steatosis in LDLR-/-AS model mice by promoting liver efferocytosis.
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