中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2008年
12期
1101-1105
,共5页
郭津%徐长庆%李鸿珠%王丽娜%王鲁川%张力%张伟华%李光伟%田野
郭津%徐長慶%李鴻珠%王麗娜%王魯川%張力%張偉華%李光偉%田野
곽진%서장경%리홍주%왕려나%왕로천%장력%장위화%리광위%전야
动脉粥样硬化%受体,钙敏感%心肌%细胞凋亡
動脈粥樣硬化%受體,鈣敏感%心肌%細胞凋亡
동맥죽양경화%수체,개민감%심기%세포조망
Atherosclerosis%Receptors,calcium-sensing%Myocardium%Apoptosis
目的 观察高脂血症和动脉粥样硬化对大鼠心肌钙敏感受体(CaSR)表达和细胞凋亡的影响.方法 采用腹腔注射维生素(Vit)D3(6×105U/kg)+高脂饮食6周的方法,建立大鼠高脂血症和动脉粥样硬化模型.Wistar大鼠随机分为正常对照组(n=12)和动脉粥样硬化组(n=12).采用RT-PCR和Western blot分别观察CaSR、Bax、Bcl-2、easpase-3的mRNA和蛋白表达.TUNEL染色观察心肌细胞凋亡情况.光镜观察腹主动脉和心肌形态学变化.电镜观察心脏超微结构变化.紫外分光法检测乳酸脱氢酶、肌酸激酶、超氧化物岐化酶的活性和丙二醛的含量,电化学免疫发光法检测肌钙蛋白水平.结果 动脉粥样硬化组乳酸脱氢酶和肌酸激酶活性、丙二醛含量和肌钙蛋白水平、细胞凋亡指数以及CaSR、Bax和caspase-3的表达均高于对照组,而超氧化物岐化酶活性则低于对照组,Bcl-2表达低于对照组,心肌细胞超微结构损伤严重.结论 高脂血症和动脉粥样硬化可引起大鼠心肌CaSR的表达增加和细胞凋亡,其机制与心肌缺血所致的氧化应激有关.
目的 觀察高脂血癥和動脈粥樣硬化對大鼠心肌鈣敏感受體(CaSR)錶達和細胞凋亡的影響.方法 採用腹腔註射維生素(Vit)D3(6×105U/kg)+高脂飲食6週的方法,建立大鼠高脂血癥和動脈粥樣硬化模型.Wistar大鼠隨機分為正常對照組(n=12)和動脈粥樣硬化組(n=12).採用RT-PCR和Western blot分彆觀察CaSR、Bax、Bcl-2、easpase-3的mRNA和蛋白錶達.TUNEL染色觀察心肌細胞凋亡情況.光鏡觀察腹主動脈和心肌形態學變化.電鏡觀察心髒超微結構變化.紫外分光法檢測乳痠脫氫酶、肌痠激酶、超氧化物岐化酶的活性和丙二醛的含量,電化學免疫髮光法檢測肌鈣蛋白水平.結果 動脈粥樣硬化組乳痠脫氫酶和肌痠激酶活性、丙二醛含量和肌鈣蛋白水平、細胞凋亡指數以及CaSR、Bax和caspase-3的錶達均高于對照組,而超氧化物岐化酶活性則低于對照組,Bcl-2錶達低于對照組,心肌細胞超微結構損傷嚴重.結論 高脂血癥和動脈粥樣硬化可引起大鼠心肌CaSR的錶達增加和細胞凋亡,其機製與心肌缺血所緻的氧化應激有關.
목적 관찰고지혈증화동맥죽양경화대대서심기개민감수체(CaSR)표체화세포조망적영향.방법 채용복강주사유생소(Vit)D3(6×105U/kg)+고지음식6주적방법,건립대서고지혈증화동맥죽양경화모형.Wistar대서수궤분위정상대조조(n=12)화동맥죽양경화조(n=12).채용RT-PCR화Western blot분별관찰CaSR、Bax、Bcl-2、easpase-3적mRNA화단백표체.TUNEL염색관찰심기세포조망정황.광경관찰복주동맥화심기형태학변화.전경관찰심장초미결구변화.자외분광법검측유산탈경매、기산격매、초양화물기화매적활성화병이철적함량,전화학면역발광법검측기개단백수평.결과 동맥죽양경화조유산탈경매화기산격매활성、병이철함량화기개단백수평、세포조망지수이급CaSR、Bax화caspase-3적표체균고우대조조,이초양화물기화매활성칙저우대조조,Bcl-2표체저우대조조,심기세포초미결구손상엄중.결론 고지혈증화동맥죽양경화가인기대서심기CaSR적표체증가화세포조망,기궤제여심기결혈소치적양화응격유관.
Objective To observe the effect of hyperlipidemia and atheroselerosis on rat myocardial expression of calcium-sensing receptor and alyJptosis.Methods The rat atherosclerosis model was induced by intraperitoneal injection of VD3(6×105U/kg)and high cholesterol diet.Wistar rats were divided into two groups:①Control group;②AS group(n=12 each).The expressions of CaSR,Bcl-2,Bax and caspase-3 were analyzed by Western blot and RT-PCR.Apoptotic cells were observed by TUNEL assay.The morphological changes of abdominal aorta and cardiac tissues were observed under optical and electro microscopes.The activity of LDH,CK,SOD and the content of MDA were assayed with ultraviolet spectrophotometer.The level of cTnT waft detected by electrochemical immunofluoresence.Results Compared with control group,the activity of LDH and CK,the content of M DA and cTnT,the apoptosis index,the expression of CaSR,Bax and caspase-3 were significantly increased,but the SOD activity and Bcl-2 expression were significantly decreased,the myocardial uhrastructure injury was significantly aggravated in the AS group(all P<0.05).Conclusion Hyperlipidemia and atherosclerosis can up-regulate myocardial calcium-sensing receptor expression,promote myocardial apoptosis,aggravate oxidative stress and myocardial ischemia.