CAJ | 학술논문

目的探讨房颤状态下大鼠心肌血管紧张素Ⅰ型(AT1R)、Ⅱ型受体(AT2R) mRNA的表达水平以及青蒿提取物对其表达的影响.方法建立房颤大鼠模型,用青蒿提取物进行干预,以卡托普利作为对照组.通过PCR、Western-blot技术观察AT1RmRNA、AT2RmRNA表达以及蛋白表达.结果与对照组(0.36±0.05)相比,模型组大鼠(0.84±0.04)心肌AT1R mRNA的表达增加(P＜0.05).青蒿组(0.56±0.03)与卡托普利组(0.53±0.04)均可减少房颤大鼠心肌AT1R mRNA的表达(P＜0.05).卡托普利组对AT1RmRNA的减少趋势较明显,但与青蒿组比较,差异无统计学意义(P＞0.05).青蒿提取物对于AT2R mRNA的表达未见影响.结论房颤大鼠AT1R的表达明显增加.青蒿提取物可有效减少房颤大鼠心肌AT1R表达.
목적 탐토방전상태하대서심기혈관긴장소Ⅰ형(AT1R)、Ⅱ형수체(AT2R) mRNA적표체수평이급청호제취물대기표체적영향.방법 건립방전대서모형,용청호제취물진행간예,이잡탁보리작위대조조.통과PCR、Western-blot기술관찰AT1RmRNA、AT2RmRNA표체이급단백표체.결과 여대조조(0.36±0.05)상비,모형조대서(0.84±0.04)심기AT1R mRNA적표체증가(P＜0.05).청호조(0.56±0.03)여잡탁보리조(0.53±0.04)균가감소방전대서심기AT1R mRNA적표체(P＜0.05).잡탁보리조대AT1RmRNA적감소추세교명현,단여청호조비교,차이무통계학의의(P＞0.05).청호제취물대우AT2R mRNA적표체미견영향.결론 방전대서AT1R적표체명현증가.청호제취물가유효감소방전대서심기AT1R표체.
Objective Through establishing a rat model of atrial fibrillation,to study myocardial angiotensin type Ⅰ (AT1R) and type Ⅱ receptor (AT2R) mRNA expression levels in of the state atrial fibrillation and Artemisia annua extract on its expression.Methods Rat model of atrial fibrillation was established,Artemisia annua extract was used for intervention and captopril was adopted as controls.AT1R,AT2R mRNA and protein expression were observed by PCR and Western-blot technology.Results Compared with the control group (0.36±0.05),myocardial AT1R mRNA expression was significantly increased in the model group (0.84±0.04) (P＜0.05).BothArtemisia annua (0.56±0.03) and captopril (0.53±0.04) could significantly reduce the myocardial AT1R mRNA expression in the atrial fibrillation rats (P＜0.05).Captopril showed obvious AT1R mRNA reduction trend,but there was statistical significance compared with Artemisinic extract (P＞0.05).Artemisinic extract showed no impact on AT2R mRNA expression.Conclusion AT1R was closely related to the incidence of atrial fibrillation.AT1R expression was significantly increased in atrial fibrillation rat.The artemisinic extract can be effectively reduced fibrillation myocardial AT1R expression,which may link with its artemisinic antiarrhythmic mechanism.