摘要
目的:探讨白藜芦醇(RES)对长时程低温保存的大鼠供心是否具有保护作用及其机制是否通过调节Sirt-1的表达。方法:SD大鼠随机分为以下7组,包括空白对照组(control),单纯9 h低温保存组(9 h),RES组(3、10、30μmol/L RES组),尼克酰胺组(NAM:保存液中加入Sirt-1抑制剂尼克酰胺NAM 40μmol/L),白藜芦醇+尼克酰胺组(RES+NAM:保存液中加入30μmol/L RES和40μmol/L NAM)。采用大鼠离体心脏Langendorff灌流模型,HE染色观察心肌细胞在各组中的形态学变化;用Real-TimePCR和Western blot法分别检测Sirt-1基因和蛋白在各组中的表达。结果:1与空白对照组相比,9 h组心肌细胞损伤明显加重,Sirt-1基因和蛋白表达均明显下调(P<0.01);2与9 h组相比,3、10、30μmol/L RES组心肌细胞损伤逐渐减轻,Sirt-1表达水平呈剂量依赖性升高(P<0.05);3RES的心肌细胞保护作用可被Sirt-1抑制剂NAM所取消。结论:RES能够改善长时程低温保存引起的心肌细胞损伤,这种保护作用可能通过上调Sirt-1的表达来实现。
Objective： To investigate whether resveratrol （RKS） plays a protective role in hypothennic preserved isolated rat hearts and whether it is mediated by regulation of silent information regulator protein-1 （Sirt-1） expression. Methods： The Langendorff model of isolated rat heart was used. After stored in different Celsior solution at 4℃for 9 h, SD rat hearts were randomly divided into 7 groups： blank control group;9 h group （soley hypothennic preservation for 9 h） ; RKS group （3,10,30 μmol/L RES treatment plus hypothermic preservation for 9 h ） ,niacinamide （NAM） group （40 μmol/L NAM added in Celsior solution plus hypothermic preservation for 9 h）,RKS ＋ NAM group （30 μmol/L RES and 40 μmol/L NAM were added in Celsior solution plus hypothermic preservation for 9 h）. The morphological changes of cardiomyocytes were detected by the HE staining with the light microscope. The mRNA and protein expression levels of Sirt-lwere detected by Real-Time PCR and Western blot respectively. Results： ①Compared with the blank control group, myocardiocytes were injured remarkably in the 9 h group and the Silt- 1 mRNA and protein expression levels were decreased significantly（ P 〈 0.01） ; ②Compared with the 9 h group, rat myocardial injury was alleviated gradually in 3,10,30 μmol/L RES group and the Sift-1 mRNA and protein expression levels were increased in a doec-dependent manner（ P 〈 0.05） ;③）The above protective effects of RES were attenuated by Sirt-1 inhibitor NAM. Conclusion： can protect myocardiocytes from injury caused by long range hypothermic preservation and this protective effect maybe mediated by uprngulation of Sift-1 expression.
出处
《中国应用生理学杂志》
CAS
CSCD
2014年第4期348-351,共4页
Chinese Journal of Applied Physiology
