Effect of Quercetin on Atherosclerosis Based on Expressions of ABCA1, LXR-α and PCSK9 in ApoE-/- Mice

Objective:To investigate the effect of quercetin on ATP binding cassette transporter A1(ABCA1),liver X receptor(LXR),and proprotein convertase subtilisin/kexin type 9(PCSK9)expressions in apoE-knockout(ApoE-/-)mice.Methods:The high-fat diet-induced atherosclerosis(AS)in ApoE-/-mice was established.Thirtysix mice were divided into 3 groups using random number table method:model group(n=12),quercetin group(n=12),and atorvastatin group(n=12),with C57BL/6J mice of the same strain and age as the control group(n=12).Quercetin group and atorvastatin group were administrated with quercetin and atorvastatin by oral gavage,with doses of 12.5 and 4 mg/(kg・d),respectively.Animals in the control and model groups were given an equal volume of distilled water by oral gavage once per day for a total of 12 weeks.Western blot and immunohistochemical methods were employed to determine the aortic ABCA1,LXR-a and PCSK9 protein expressi on.En zyme linked imm uno sorbent assay method was used to detect the expressi on of serum total cholesterol(TC),triglyceride(TG),high density lipoprotein-cholesterol(HDL-C),low density lipoproteincholesterol(LDL-C),tumor necrosis factor-a(TNF-a),interleukin-6(IL-6),and IL-10,combined with tissue pathological exami nation.Results:ApoE-/-mice fed with a high-fat diet had no table atherosclerosis lesions,with reduced ABCA1,LXR-a and IL-10 levels(all P<0.01),elevated PCSK9,TNF-a and IL-6 expression,and increased TC and LDL-C con tents(all P<0.01).After querceti n in terventi on,the areas of AS plaques and the expressions of PCSK9,TNF-a and IL-6 were significantly reduced(all P<0.01),while the expressions of ABCA1 and LXR-a were increased significantly(all P<0.01).Conclusion:Quercetin effectively interfered with AS development by regulating the expressions of ABCA1,LXR-a and PCSK9 in ApoE,mice.

Objective: To investigate the effect of quercetin on ATP binding cassette transporter A1（ABCA1）, liver X receptor（LXR）, and proprotein convertase subtilisin/kexin type 9（PCSK9） expressions in apo E-knockout(Apo E-/- ) mice. Methods: The high-fat diet-induced atherosclerosis（AS） in Apo E-/- mice was established. Thirtysix mice were divided into 3 groups using random number table method: model group（n=12）, quercetin group（n=12）, and atorvastatin group（n=12）, with C57 BL/6 J mice of the same strain and age as the control group（n=12）. Quercetin group and atorvastatin group were administrated with quercetin and atorvastatin by oral gavage, with doses of 12.5 and 4 mg/（kg·d）, respectively. Animals in the control and model groups were given an equal volume of distilled water by oral gavage once per day for a total of 12 weeks. Western blot and immunohistochemical methods were employed to determine the aortic ABCA1, LXR-α and PCSK9 protein expression. Enzyme linked immunosorbent assay method was used to detect the expression of serum total cholesterol（TC）, triglyceride（TG）, high density lipoprotein-cholesterol（HDL-C）, low density lipoproteincholesterol（LDL-C）, tumor necrosis factor-α（TNF-α）, interleukin-6（IL-6）, and IL-10, combined with tissue pathological examination. Results: Apo E-/- mice fed with a high-fat diet had notable atherosclerosis lesions, with reduced ABCA1, LXR-α and IL-10 levels（all P<0.01）, elevated PCSK9, TNF-α and IL-6 expression, and increased TC and LDL-C contents（all P<0.01）. After quercetin intervention, the areas of AS plaques and the expressions of PCSK9, TNF-α and IL-6 were significantly reduced（all P<0.01）, while the expressions of ABCA1 and LXR-α were increased significantly（all P<0.01）. Conclusion: Quercetin effectively interfered with AS development by regulating the expressions of ABCA1, LXR-α and PCSK9 in Apo E-/- mice.