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Objective:To explore the correlation between FcγRⅢA(CD16A) and aortic atherosclerotic plaque destabilization in apoE knockout(apoE KO) mice and the intervention effects of effective components of Chuanxiong Rhizome and Red Peony Root Methods:Eight 8-week-old male C57BL/6J mice were selected as the control group.Forty 8-week-old male apoE KO mice were randomly divided into the model group,apoE KO + intraperitoneal injection immunoglobulin group(IVIG),apoE KO + simvastatin group(Sm),apoE KO + high dosage of Xiongshao Capsule(XSC,芎芍胶囊) group(XSCH),and apoE KO + low dosage of XSC group (XSCL),8 mice in each group.Mice in the control group were put on a normal diet,and others were fed with a high-fat diet.After 10-week different interventions,monocyte CD16 expression was detected by flow cytometry, aortic matrix metalloproteinase-9(MMP-9) mRNA expression was detected using reverse transcription-polymerase chain reaction,and serum tumor necrosis factor(TNF)-αlevel was detected using enzyme-linked immunosorbent assay.Results:Compared with the control group,monocyte CD16 expression,aortic MMP-9 mRNA expression,and serum TNF-αlevel in the model group increased obviously(P<0.01).Injections of apoE KO mice with intraperitoneal immunoglobulin during a 5-day period significantly reduced the monocyte CD16 expression,aortic MMP-9 mRNA expression,and serum TNF-αlevel(P<0.01 or 0.05) over a 10-week period of high-fat diet.Indices above in the Sm group,XSCH group,and XSCL group decreased in a different degree. Of them,the aortic MMP-9 mRNA expression in XSCH group was lower than that in Sm group(P<0.05) and the monocyte CD16 expression and serum TNF-αlevel showed no significant difference between XSCH group and Sm group(P>0.05).Correlation analyses suggested positive correlation between monocyte CD16 expression and aortic MMP-9 mRNA expression or serum TNF-αlevel in IVIG group,XSCH group,and XSCL group. Conclusions:FcγRⅢA mediates systemic inflammation in the progression of coronary heart disease with blood stasis syndrome.XSC could stabilize atherosclerotic plaque by suppressing inflammation and its target was relative with FcγRⅢA.