中华老年心脑血管病杂志
中華老年心腦血管病雜誌
중화노년심뇌혈관병잡지
CHINESE JOURNAL OF GERIATRIC CARDIOVASCULAR AND CEREBROVASCULAR DISEASES
2014年
6期
627-629
,共3页
李艳芳%蒋志丽%郭彦青%宋俊迎
李豔芳%蔣誌麗%郭彥青%宋俊迎
리염방%장지려%곽언청%송준영
受体 ,肾上腺素能β3%载脂蛋白E类%前蛋白转化酶类%受体 ,LDL%降血脂药
受體 ,腎上腺素能β3%載脂蛋白E類%前蛋白轉化酶類%受體 ,LDL%降血脂藥
수체 ,신상선소능β3%재지단백E류%전단백전화매류%수체 ,LDL%강혈지약
receptors,adrenergic,beta-3%apolipoproteins E%proprotein convertases%receptors,LDL%antilipemic agents
目的:观察激动β3肾上腺素受体(β3-AR)对载脂蛋白E基因敲除(apoE-/-)老年高脂小鼠血脂、肝脏前蛋白转化酶枯草溶菌素9(PCSK9)和LDL 受体(LDLR)表达水平的影响。方法选择10周龄雄性C57BL/6小鼠10只(A组)。apoE-/-小鼠40只给予高脂饲料饲养至36周龄,随机分为4组,分别为高脂模型组(B组)、阿托伐他汀阳性药物对照组(C组)、β3-A R激动剂小剂量组(D组)、β3-A R激动剂大剂量组(E组),每组10只,共干预12周。采用Beckman CX7全自动生化分析仪,检测血清 TC、TG、VLDL/LDL-C、HDL-C水平,采用Western blot测定肝脏PCSK9和LDLR表达水平。结果与B组比较,C组、D组和E组 TC、VLDL/LDL-C明显下降,C组、B组、D组LDLR水平明显上调,C组PCSK9水平明显上调(P<0.05,P<0.01);与C组比较,D组和E组TG、PCSK9水平明显下降,D组LDLR水平明显下降,HDL-C水平明显升高,差异有统计学意义(P<0.05,P<0.01)。结论β3-AR调脂、升高LDLR、降低PCSK9表达水平是其抗动脉粥样硬化的多重作用机制之一。
目的:觀察激動β3腎上腺素受體(β3-AR)對載脂蛋白E基因敲除(apoE-/-)老年高脂小鼠血脂、肝髒前蛋白轉化酶枯草溶菌素9(PCSK9)和LDL 受體(LDLR)錶達水平的影響。方法選擇10週齡雄性C57BL/6小鼠10隻(A組)。apoE-/-小鼠40隻給予高脂飼料飼養至36週齡,隨機分為4組,分彆為高脂模型組(B組)、阿託伐他汀暘性藥物對照組(C組)、β3-A R激動劑小劑量組(D組)、β3-A R激動劑大劑量組(E組),每組10隻,共榦預12週。採用Beckman CX7全自動生化分析儀,檢測血清 TC、TG、VLDL/LDL-C、HDL-C水平,採用Western blot測定肝髒PCSK9和LDLR錶達水平。結果與B組比較,C組、D組和E組 TC、VLDL/LDL-C明顯下降,C組、B組、D組LDLR水平明顯上調,C組PCSK9水平明顯上調(P<0.05,P<0.01);與C組比較,D組和E組TG、PCSK9水平明顯下降,D組LDLR水平明顯下降,HDL-C水平明顯升高,差異有統計學意義(P<0.05,P<0.01)。結論β3-AR調脂、升高LDLR、降低PCSK9錶達水平是其抗動脈粥樣硬化的多重作用機製之一。
목적:관찰격동β3신상선소수체(β3-AR)대재지단백E기인고제(apoE-/-)노년고지소서혈지、간장전단백전화매고초용균소9(PCSK9)화LDL 수체(LDLR)표체수평적영향。방법선택10주령웅성C57BL/6소서10지(A조)。apoE-/-소서40지급여고지사료사양지36주령,수궤분위4조,분별위고지모형조(B조)、아탁벌타정양성약물대조조(C조)、β3-A R격동제소제량조(D조)、β3-A R격동제대제량조(E조),매조10지,공간예12주。채용Beckman CX7전자동생화분석의,검측혈청 TC、TG、VLDL/LDL-C、HDL-C수평,채용Western blot측정간장PCSK9화LDLR표체수평。결과여B조비교,C조、D조화E조 TC、VLDL/LDL-C명현하강,C조、B조、D조LDLR수평명현상조,C조PCSK9수평명현상조(P<0.05,P<0.01);여C조비교,D조화E조TG、PCSK9수평명현하강,D조LDLR수평명현하강,HDL-C수평명현승고,차이유통계학의의(P<0.05,P<0.01)。결론β3-AR조지、승고LDLR、강저PCSK9표체수평시기항동맥죽양경화적다중작용궤제지일。
Objective To study the effect of β3-AR agonists on expression of PCSK9 and LDLR in elderly apoE gene knock-out mice .Methods Ten male C57BL/6 mice aged 10 weeks served as group A and 40 apoE gene knock-out mice fed with high fat diet to 36 weeks old were randomly divided into high fat model group (group B) ,positive atrovastatin control group (group C) ,small doseβ3-AR agonist group (group D) and large dose β3-AR agonist group (group E) ,10 in each group .The animals were treated with atorvastatin and β3-AR agonists for 12 weeks .Serum levels of TC ,TG ,VLDL/LDL-C ,HDL-C were measured with the Beckman CX7 automatic biochemical analyzer and expression of PCSK9 and LDLR was detected by Western blot .Results The serum TC and VLDL/LDL-C levels were significantly lower in groups C ,D and E than in group B ,the expression level of LDLR was significantly higher in groups C ,B and D than in group E while that of PCSK9 was significantly higher in group C than in groups B ,D and E (P<0 .05 ,P<0 .01) .The serum TG level was significantly lower in groups D and E than in group C ,the expression level of LDLR was significantly lower while the serum HDL-C level was significantly higher in group D than in group C (P<0 .05 ,P<0 .01) .Conclusion β3-AR agonist decreases TC ,VLDL/LDL-C , TG levels and expression of PCSK9 ,and increases LDLR and HDL-C level ,which are one of its anti-atherosclerosis mechanisms in elderly apoE-/-mice .