褪黑素对糖尿病大鼠心肌转化生长因子-β1表达的影响

糖尿病(DM)心肌病是DM患者所特有的心脏病变，其病理特点是心肌细胞肥大、心肌纤维化和心肌微小血管广泛内膜病变。转化生长因子β1(TGF-β1)对细胞的生长、分化和免疫功能都有重要的调节作用。动物试验表明体内转染TGF-β1基因可促进心肌纤维化。Doi等用免疫组化方法证实，DM大鼠心脏TGF-β1表达显著增高。褪黑素(Me     

NF-κB、TGF-β1在糖尿病大鼠心肌及主动脉中的表达

目的:探讨链脲佐菌素(STZ)诱导的糖尿病(DM)大鼠心肌及主动脉核转录因子-κB(NF-κB)、转化生长因子-β1(TGF-β1)的表达。方法:用HE及MASSON染色观察DM大鼠心肌及主动脉的病理改变,用免疫组化的方法检测上述免疫因子的表达。结果:DM大鼠心肌、主动脉NF-κB、TGF-β1表达均明显高于正常对照组(CON),差异有统计学意义(P0.01)。结论:NF-κB和TGF-β1在DM心血管并发症的发生发展机制中起重要作用。     

贝那普利下调TGF-β1及Bax表达对糖尿病大鼠心肌的保护作用

目的 探讨贝那普利(BZ)对糖尿病(DM)大鼠心肌转化生长因子β1(TGF-β1)和Bax的表达及心肌肥厚指标的影响.方法 SD大鼠腹腔注射链脲佐菌素(STZ)制备DM模型.实验分为正常对照组(CON)、DM组和BZ治疗组(BZ).治疗组每日灌胃给予贝那普利(10 mg·kg-1·d-1).8 w后测定心脏质量指数(HMI)、左心室质量指数(LVMI),并取左心室心肌免疫组化法检测TGF-β1和 Bax在心肌组织中的表达,透射电镜观察心肌组织超微结构变化.结果 与CON组相比,DM组大鼠HMI、LVMI明显升高;心肌TGF-β1和 Bax蛋白表达显著增强(P＜0.05,P＜0.01);电镜发现DM心肌细胞肿胀、肌丝稀疏,线粒体变性肿胀,间质胶原增生及微血管基底膜增厚.与DM组相比,BZ干预后,HMI、LVMI明显降低(P＜0.01);心肌TGF-β1和 Bax蛋白表达减弱(P＜0.01);心肌超微结构改变减轻.结论 TGF-β1 可能通过刺激促凋亡因子Bax表达诱导心肌细胞凋亡,促进DM心肌肥厚.BZ能在一定程度上抑制TGF-β1和Bax的表达从而延缓DM心肌病理进程.     

银丹心脑通软胶囊对大鼠急性心肌梗死后心肌组织TGF-β1表达的影响

目的观察银丹心脑通软胶囊对大鼠急性心肌梗死(AMI)后心肌组织非梗死区转化生长因子β1(TGF-β1)表达的影响。方法用结扎左冠状动脉前降支方法制成大鼠AMI模型,造模成功后将大鼠随机分为5组,银丹大剂量组(12只),给予银丹心脑通软胶囊1.6g/(kg·d)灌胃,银丹小剂量组(12只),给予银丹心脑通软胶囊0.8g/(kg·d)灌胃,阳性药卡托普利(开博通)对照组(12只),开博通5mg/(kg.d)灌胃,假手术组(只穿线不结扎,10只)、梗死模型组(MI组,12只),假手术组与梗死模型组给予同等剂量生理盐水。在梗死后4周剪取心脏标本,用反转录-聚合酶链式反应(RT-PCR)检测非梗死区心肌TGF-β1 mRNA的表达,计算左心室重量及心脏重量指数,行HE染色观察心肌组织学改变。结果与假手术组比较,4周后MI组左心室重量及心脏重量指数显著升高,心肌组织非梗死区TGF-β1 mRNA表达水平亦明显升高(P<0.01);各给药组与MI组比较均可显著减低心室重量及心脏重量指数及TGF-β1 mRNA表达水平,银丹心脑通软胶囊的作用强度与剂量呈正相关。结论TGF-β1参与了心肌梗死后心室重构过程,银丹心脑通软胶囊能够减低梗死后左室重量及心脏重量指数及减少TGF-β1的表达,能够改善梗死后的心室重构。     

Ⅱ型糖尿病大鼠心肌梗死后交感神经重构与神经生长因子(NGF)的表达改变

目的:探讨糖尿病并发心肌梗死(MI)对大鼠心肌中神经生长因子(NGF)的表达及交感神经再生重构的影响。方法:将实验大鼠分为正常对照组、糖尿病对照组、MI对照组及糖尿病MI组,从各组大鼠的左心室梗死周边、室间隔和右心室取材,通过免疫组化染色并结合计算机图像处理技术,对心肌中NGF蛋白表达及交感神经支配进行对比分析。结果:与正常对照组及糖尿病心梗组比较,MI对照组的NGF表达均增加(均P0.05),交感神经支配密度也均明显增加(均P0.01),并且二者在梗死周边、室间隔及右心室3个部位的表达存在相关性(均P0.05),糖尿病对照组的NGF表达均降低(P0.05,P0.01),交感神经支配密度分别为无明显差异及明显降低(P0.01)。结论:糖尿病可抑制心肌细胞表达NGF,但却可促进MI后交感神经的过度再生与重构。推测糖尿病条件下,NGF并非交感神经再生重构的决定因素,尚存在其他途径对交感神经再生及重构进行调节。     

糖尿病心肌病心肌细胞纤维化的病理改变

目的研究糖尿病(DM)大鼠不同病程心肌纤维化及其相关病理变化。方法选取18只DM心肌模型后大鼠随机分为DM大鼠1个月组(DM1组)、3个月组(DM3组)、6个月组(DM6组),每组6只。另选18只健康大鼠作为对照组。采用氯胺T法测定羟脯氨酸含量,为心肌胶原总含量。免疫组织化学染色测定心肌胶原蛋白Ⅰ、Ⅲ和心肌细胞心肌型α肌动蛋白(α-actin)及转化生长因子β1(TGF-β1)平均积分吸光度(A)。光镜和透射电镜下观察心肌病理变化。结果DM6组心肌胶原总含量明显高于DM1组和DM3组(P<0.01)。与对照组比较,DM3组心肌胶原蛋白Ⅰ表达伴随TGF-β1的表达开始明显增加(P<0.01)。心肌细胞心肌型α-actin表达较对照组明显减少(P<0.01)。各组大鼠心肌横切面可见粗大胶原纤维相互连接成网状,排列紊乱,分布不匀。α-actin表达明显减少,有糖原沉积现象。结论胶原蛋白Ⅰ呈现持续性增加是DM大鼠心肌纤维化的主要原因。TGF-β1参与了心肌纤维化发生的早期过程。糖原沉积和心肌细胞心肌型α-actin表达减少是DM心肌病的病理基础。     

卡托普利及合用氯沙坦对大鼠心肌梗死区肌纤维细胞增殖和功能的影响

目的:比较卡托普利组和卡托普利与氯沙坦合用组急性心肌梗死(AMI)大鼠心肌瘢痕组织的肌纤维细胞在离体情况下的增殖率及转化生长因子-1(TGF-β1)水平。方法:雄性wistar大鼠36只,前降支结扎术后存活12h以上者随机分成对照组、卡托普利组和合用组,用药14d后分离培养梗死区肌纤维细胞。流式细胞技术检测血管紧张素Ⅱ(AngⅡ),刺激前后S期细胞比率(SPF)和增殖指数(PI),酶联免疫吸附实验(ELASA)法检测培养液中TGF-β1浓度。结果:AMI后梗死区肌纤维细胞具有极高的增殖活性。合用组SPF/PI低于对照组,而卡托普利组与对照组相比无统计学意义。合用组培养液中TGF-β1浓度低于对照组和卡托普利组。各组肌纤维细胞对AngⅡ刺激的反应性无统计学意义。结论:AMI后早期在有效剂量卡托普利的基础上加用氯沙坦更强抑制梗死区肌纤维细胞的增殖能力和生长因子产生。     

芪丹通脉片对心肌梗死后大鼠心肌纤维化重构的影响

目的:观察益气活血复方芪丹通脉片（qidan tongmai tablet,QDTMT）对大鼠心肌梗死(MI)后心功能及左心室非梗死区心肌纤维化的影响。方法: 以结扎SD大鼠左冠脉前降支法建立MI模型,随机分为假手术(Sham)组、MI组、MI+QDTMT小剂量(MI-QDTMTL)组和MI+QDTMT大剂量(MI-QDTMTH)组。术后24 h各组均用生理盐水配制成等体积药液灌胃4周,4周后以多普勒超声评价心脏功能;测定心室的质量/体质量(HW/BW);以MASSON染色检测非梗死区胶原的含量;用RT-PCR法检测非梗死区转化生长因子-β1（TGF-β1）、Ⅰ型胶原蛋白（Collagen type 1,Col1）及Ⅲ型胶原蛋白（Collagen type 3,Col3）mRNA的表达水平。采用大鼠羟脯氨酸（HYP）的ELASA试剂盒检测非梗死区中HYP的含量。结果: ①术后4周心功能:与MI组比较,MI-QDTMTL组和MI-QDTMTH组左室舒张末期内径(LVEDD)和HW/BW均降低,而射血分数(EF)升高（P<0.01或P<0.05）;②非梗死区心肌胶原蛋白的含量: MI-QDTMTL组胶原和MI-QDTMTH组胶原含量均低于MI组（P<0.01）;MI-QDTMTH组胶原的含量明显低于MI-QDTMTL组(P<0.01);③非梗死区TGF-β1、Col1、Col3mRNA的表达:与MI组比较,MI-QDTMTL组、MI-QDTMTH组的TGF-β1 Col1、Col3 mRNA均显著降低(P<0.01或P<0.05);MI-QDTMTH组TGF-β1、Col1、Col3 mRNA的表达显著低于MI-QDTMTL组(P<0.05);④非梗死区HYP的含量: MI-QDTMTL组与MI-QDTMTH组HYP的含量低于MI组(P<0.05,P<0.01); MI-QDTMTH组HYP的含量低于MI-QDTMTL组(P<0.05)。结论: QDTMT通过下调MI交界区TGF-β1、Col1、Col3 mRNA的表达及HYP产生,进而抑制MI后非梗死区反应性胶原的过度沉积,且高剂量组比低剂量组的疗效更好,为防治MI后非梗死区心肌纤维化重构,改善心脏功能提供了新的治疗思路。     

卡维地洛对心肌梗死后大鼠心肌细胞因子表达及心室重塑的影响

目的探讨细胞因子在心肌梗死(MI)后大鼠心室重塑中的作用,以及卡维地洛对心肌细胞因子表达和心室重塑的影响。方法结扎大鼠左冠状动脉前降支建立MI模型,随机分为对照组和卡维地洛组,另设假手术组。卡维地洛组给予卡维地洛灌胃,对照组和假手术组仅以等体积生理盐水灌胃,观察4周末卡维地洛对心肌细胞肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)、转化生长因子β1(TGF-β1)和白介素-10(IL-10)mRNA的表达及心室重塑的影响。结果MI后4周末大鼠心肌细胞因子表达(梗死区:TNF-α1.07±0.23、IL-1β1.07±0.36、IL-61.25±0.47、TGF-β11.25±0.16I、L-100.84±0.06;非梗死区:TNF-α1.05±0.09I、L-1β1.04±0.14、IL-61.04±0.13、TGF-β11.05±0.07I、L-100.77±0.09)较假手术组明显增加(P<0.01)。与对照组比较,卡维地洛组血液动力学指标及心室重塑改善,心肌致炎性细胞因子mRNA表达(梗死区:TNF-α0.58±0.06I、L-1β0.71±0.08I、L-60.63±0.08;非梗死区TNF-α0.67±0.19、IL-1β0.58±0.11、IL-60.59±0.15)和致纤维化性细胞因子TGF-β1mRNA表达(梗死区0.72±0.14,非梗死区0.73±0.16)降低,而抗炎性细胞因子IL-10mRNA表达差异无统计学意义。结论细胞因子可能参与了MI后心室重塑。卡维地洛改善心室重塑的作用机制至少部分与对细胞因子基因表达作用有关。     

内皮祖细胞移植治疗大鼠急性心肌梗死的实验研究

目的探讨大鼠内皮祖细胞(EPCs)移植于梗死心肌的增殖分化情况及对心功能的影响。方法分离培养大鼠EPCs,免疫荧光法检测其CD34+、CD133+和Flk-1+的表达。将SD大鼠冠状动脉左前降支结扎制造急性心肌梗死模型后,在梗死心肌处植入DAPI标记的EPCs(实验组)或M 199培养液(对照组)。移植后1周及4周,心脏超声检查心功能,并对梗死区心肌组织进行移植细胞形态学检查及毛细血管密度测定,逆转录聚合酶链反应及酶联免疫吸附测定梗死周边区血管内皮生长因子(VEGF)的表达。结果培养获得EPCs,其表型为CD34+、CD133+和Flk-1+。植入梗死区的EPCs可以分化为血管内皮细胞,实验组梗死心肌处血管密度较对照组明显增高(P<0.01),并且VEGF基因及蛋白表达在移植后1周均较对照组明显增高(P<0.01)。移植后4周,实验组大鼠左心室射血分数及左心室短轴缩短率较对照组明显提高(P<0.01);而移植后1周,两组大鼠超声检测心功能各指标变化不明显。结论同种异体EPCs移植到梗死心肌大鼠缺血心肌能分化为毛细血管内皮细胞,促进梗死后心肌血管新生,改善心功能。     

Sustained cardiomyocyte apoptosis and left ventricular remodelling after myocardial infarction in experimental diabetes

Aims/hypothesis Diabetes is known to reduce survival after myocardial infarction. Our aim was to examine whether diabetes is associated with enhanced cardiomyocyte apoptosis and thus interferes with the post-infarction remodelling process in myocardium in rat.Methods Four weeks after intravenous streptozotocin (diabetic groups) or citrate buffer (controls) injection, myocardial infarction was produced by ligation of left descending coronary artery. Level of cardiomyocyte apoptosis was quantified by TUNEL and caspase-3 methods. Collagen volume fraction and connective tissue growth factor were determined under microscope. Left ventricular dimensions were evaluated by echocardiography and planimetry.Results The number of apoptotic cardiomyocytes was equally high in diabetic and non-diabetic rats after 1 week from infarction. At 12 weeks after infarction the number of apoptotic cells was higher in the diabetic as compared to non-diabetic rats both in the border zone of infarction and in non-infarcted area. Correspondingly, left ventricular end diastolic diameter, relative cardiac weight, connective tissue growth factor-expression and fibrosis were increased in diabetic compared with non-diabetic rats with myocardial infarction.Conclusion/interpretation Sustained cardiomyocyte apoptosis, left ventricular enlargement, increased cardiac fibrosis and enhanced profibrogenic connective tissue growth factor expression were detected after myocardial infarction in experimental diabetes. Apoptotic myocyte loss could be an important mechanism contributing to progressive dilatation of the heart and poor prognosis after myocardial infarction in diabetes.Abbreviations STZ streptozotozin - MI myocardial infarction - CTGF connective tissue growth factor - LV left ventricular - LVEDD LV end-diastolic diameter - BNP B-type natriuretic peptide     

缬沙坦对2型糖尿病大鼠心肌细胞凋亡的影响

目的探讨缬沙坦对糖尿病大鼠心肌细胞凋亡的作用。方法随机选择29只健康雄性SD大鼠中的21只,以高糖高脂饲料喂养4周后腹腔注射链脲佐菌素30mg/kg,3d后测血糖≥16.7mmol/L者（n=19）入选糖尿病大鼠模型,并随机分为糖尿病组（DM组,n=9）和缬沙坦治疗组（VAL组,n=10）,另外8只健康雄性SD大鼠为对照组（CN组,n=8）。VAL组给予缬沙坦（20mg/kg.d）治疗6周,检测各组大鼠血生化和胰岛素水平,各组大鼠于第12周末处死,取部分左心室前壁组织以TUNEL法检测大鼠心肌细胞凋亡,免疫组化法检测Caspase-3、NF-κB的表达。结果与CN组相比,DM组和VAL组大鼠心肌细胞凋亡及Caspase-3和NF-κB的阳性表达显著增多,差异具有统计学意义（P〈0.05）;与DM组相比,VAL组大鼠心肌细胞凋亡及Caspase-3和NF-κB的阳性表达明显减少,差异具有统计学意义（P〈0.05）。结论缬沙坦能够抑制糖尿病大鼠心肌细胞的凋亡,具有心肌保护作用。     

重组人生长激素对心肌梗死大鼠心功能及心肌炎性因子表达的影响

目的 观察重组人生长激素(rhGH)对大鼠急性心肌梗死后心功能及心肌炎性因子表达的影响. 方法 结扎大鼠左冠状动脉前降支建立心肌梗死模型,将术后24 h存活的大鼠随机分为对照组和rhGH组,另设假手术组.rhGH组给予rhGH 2 mg.kg-1.d-1皮下注射,对照组和假手术组给予等体积的生理盐水皮下注射,4周后观察rhGH对大鼠心功能及心肌细胞肿瘤坏死因子-α(TNF-α)、白介素-1p(IL-1p)、白介素-6(IL-6)、白介素-10(IL-10)mRNA表达的影响. 结果 与假手术组比较,对照组心肌组织中促炎性细胞因子TNF-α、IL-1β、IL-β和IL-10 mRNA表达(假手术组分别为0.10±0.02、0.08±0.01、0.18±0.01和0.14±0.05;梗死区分别为0.77±0.15、0.93±0.17、1.10±0.14和0.73±0.11;非梗死区分别为0.88±0.14、0.95±0.17、1.18±0.11和0.83±0.16)明显升高.与对照组比较,rhGH组心肌组织中TNF-α、IL-1β、IL-6 mRNA表达(梗死区分别为0.35±0.10、0.36±0.10、0.43±0.11;非梗死区分别为0.51±0.10、0.42±0.11、0.51±0.12)明显下降,IL-10 mRNA表达(梗死区为1.18±0.18;非梗死区为1.21±0.22)升高,P＜0.05.心脏超声显示rhGH组左室功能明显改善. 结论 早期rhGH治疗改善了心肌梗死大鼠心肌炎性因子表达和心脏功能.rhGH有效改善心功能与其降低心肌细胞促炎细胞因子和升高抗炎因子的作用有关.     

The impaired tolerance of the recently infarcted rat heart to cardioplegic arrest: the protective effect of orotic acid

After myocardial infarction, a reduced mass of non-infarcted myocardium remains to maintain cardiac output. This acutely stressed, non-infarcted myocardium exhibits many metabolic disturbances, and undergoes a process of acute hypertrophy. These stress-induced disturbances may reduce the tolerance of the heart to the global ischaemia of cardioplegic arrest and may explain the increased mortality and morbidity associated with cardiac surgery in patients with recent myocardial infarction. We postulated that orotic acid, a pyrimidine precursor which augments the rate of protein synthesis during hypertrophy, might improve the response of the recently infarcted heart to cardioplegic arrest. Myocardial infarction was induced in rats by coronary ligation, and after 2 days or 3 days the hearts were excised and perfused on the working heart apparatus. After measurement of work capacity, the hearts underwent 1 hour of hypothermic cardioplegic arrest. Post-arrest function was then measured and expressed as a percentage of the pre-arrest value. A group of sham-operated, non-infarcted hearts served as controls. There were two distinct findings: (1) when subjected to hypothermic cardioplegic arrest 2 days after myocardial infarction, hearts recovered only 49% of pre-arrest function, compared with 80% recovery in non-infarcted controls (P less than 0.001). Three days after infarction, recovery had improved to 68% (P less than 0.01 vs. 2 days, P less than 0.05 vs. non-infarcted). (2) Treatment with oral orotic acid following infarction augmented recovery from cardioplegic arrest to 83%, 2 days after infarction (P less than 0.001 vs. untreated) and to 87%, 3 days after infarction (P less than 0.01 vs. untreated).(ABSTRACT TRUNCATED AT 250 WORDS)     

Differences in time course of myocardial mRNA expression in non-infarcted myocardium after myocardial infarction

In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca²⁺ transport protein, such as sarcoplasmic reticulum Ca²⁺(SR-Ca²⁺)-ATPase, Na⁺-Ca²⁺ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca ²⁺ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ration of E wave to A wave velocity. Expression of myocardial α-skeletal actin, β-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca²⁺-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na⁺-Ca²⁺ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling. Received: 9 August 1999, Returned for revision: 16 September 1999, Revision received: 5 January 2000, Accepted: 26 January 2000     

PCI术后AMI患者非梗死区冠脉血流储备的变化及其对左室功能的影响

目的 观察和分析急性心肌梗死（AMI）患者PCI术后非梗死区冠脉血流储备（CFR）的变化及其对左室功能的影响。方法 22名AMI患者PCI术后1周行二维超声心动图和多巴酚丁胺负荷实时心肌声学造影（MCE）检查,测量左室功能和梗死区、非梗死区CFR,比较非梗死区CFR与梗死区及正常对照组CFR;根据非梗死区CFR值将患者分为两组,比较两组远期左室功能的变化。结果 非梗死区CFR值与正常对照组相比明显下降,非梗死区CFR与左室舒张末期容积呈负相关。结论 AMI后非梗死区心肌同样存在微循环功能障碍,非梗死区CFR值能预测AMI后远期左室功能。     

Decreased expression of Na+/H+ exchanger isoform 1 (NHE1) in non-infarcted myocardium after acute myocardial infarction

Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.     

白藜芦醇对糖尿病大鼠心脏缺血再灌注损伤的保护作用

目的探讨白藜芦醇(RSV)对糖尿病大鼠心肌缺血再灌注(MI/R)损伤的保护作用及其机制。方法通过腹腔注射链脲佐菌素诱导2型糖尿病大鼠模型。2周后糖尿病大鼠随机分为假手术(Sham)组、MI/R组和白藜芦醇(RSV)组。通过结扎左冠状动脉前降支诱导MI/R损伤模型。测定各组大鼠乳酸脱氢酶(LDH)、肌酸激酶(CK)、心肌肌钙蛋白I(cTnI)、心肌梗死面积、心脏收缩和舒张功能;TUNEL法检测心肌细胞凋亡指数;Western blot检测沉默信息调节因子1(SIRT1)、p53、乙酰化p53(Acetyl-p53)、Bcl-2、Bax以及细胞浆和线粒体细胞色素C(Cyt C)和凋亡诱导因子(AIF)的表达;HE染色检测心肌损伤评分。结果与Sham组相比,MI/R组心肌梗死面积、心肌损伤评分、心肌LDH、CK、cTnI、Acetyl-p53、Bax、细胞浆Cyt C和AIF表达以及心肌细胞凋亡指数均明显增加,而心脏收缩和舒张功能明显降低,Bcl-2和SIRT1表达以及线粒体Cyt C和AIF表达明显减少。与MI/R组相比,RSV组心肌梗死面积、心肌损伤评分、心肌LDH、CK、cTnI、Acetyl-p53、Bax、细胞浆Cyt C和AIF表达以及心肌细胞凋亡指数均明显降低,而心脏收缩和舒张功能明显改善,Bcl-2和SIRT1表达以及线粒体Cyt C和AIF表达明显增加。3组之间p53表达无差异。结论白藜芦醇可通过抗凋亡作用减轻糖尿病大鼠MI/R损伤,其作用机制与SIRT1/p53信号通路相关。