Protective effects of melatonin against myocardial injury induced by isoproterenol in rats

This study was performed to determine whether melatonin could have a protective effect against myocardial injury (MI) induced by isoproterenol (ISO) in rats. Twenty-four rats were divided into three treatment groups: (1) control (n = 8): saline solution. (2) ISO (n = 8): ISO only. (3) melatonin + ISO (n = 8). Melatonin (10 mg/kg/day, i.p.) was administered 30 min before the initiation of ISO (150 mg/kg/day, s.c.). Drugs and saline were given at 14:00 hr for two consecutive days. At the end of the second day, blood samples were taken from the abdominal aorta shortly after the rats were anesthetized for the purpose of measuring cardiac troponins T (cTnT) and I (cTnI); hearts were removed, preserved and examined microscopically. Additionally, based on the histological changes in myocardial tissue, the rats were divided into three groups: no change, mild changes and moderate and/or marked changes. The mean cTnT and cTnI values were significantly increased in ISO group compared with control group [(1.29 +/- 0.22 ng/mL versus 0.46 +/- 0.07 ng/mL, P < 0.0001) and (0.56 +/- 0.11 ng/mL versus 0.21 +/- 0.01 ng/mL, P < 0.001)], respectively, and were significantly reduced in the ISO + melatonin group (0.65 +/- 0.06 ng/mL for cTnT and 0.25 +/- 0.01 ng/mL for cTnI) compared with the ISO only group (P < 0.01), respectively. cTnT and cTnI values were significantly increased in rats with moderate and/or marked cardiac changes compared with hearts where there were mild changes and no change (P < 0.05). ISO + melatonin group showed less histological changes than the ISO group (P < 0.01). In conclusion, this study revealed a protective effect of melatonin against ISO-induced MI in rats, and its potential clinical application in the treatment of MI.     

非诺贝特对大鼠心肌损伤保护作用的实验观察

目的探讨非诺贝特对异丙基肾上腺素所致大鼠急性心肌缺血性损伤的保护作用。方法应用异丙基肾上腺素复制大鼠急性心肌缺血性损伤的动物模型,Wister大鼠随机分为3组,正常对照组、模型组(Iso)、非诺贝特保护组(FF),观察非诺贝特对大鼠心肌的形态学,血清肌酸激酶和乳酸脱氢酶(CK,LDH)以及一氧化氮(NO)的影响。结果非诺贝特能对抗异丙基肾上腺素所致的大鼠急性心肌缺血性损伤,可使其病理损伤性改变减轻,抑制CK和LDH的释放,增加NO的产生。结论非诺贝特对异丙基肾上腺素所致大鼠急性心肌缺血性损伤具有保护作用。     

Protective effects of berberine against exhaustion exercise induced myocardial injury in rats

<正>Objective To investigate the effect and possible mechanism of berberine(Ber) on myocardial injury induced by exhaustion exercise(Ee).Methods Forty healthy male SPF Sprague-Dawley rats were randomly divided into 5 groups using the random unit group design method:control group,Ee group and Ee plus Ber group     

缬沙坦对脓毒症大鼠心肌损伤保护的实验研究

目的本研究旨在观察大鼠盲肠结扎穿孔(CLP)脓毒症模型中心肌损伤的发生情况,应用血管紧张素1受体(AT1R)拮抗剂缬沙坦进行干预,观察其对心肌肾素-血管紧张素系统(RAS)包括血浆、心肌血管紧张素Ⅱ(AngⅡ)和心肌组织AT1R/AT2RmRNA表达的影响及对脓毒症大鼠心肌损伤的保护作用。方法73只Wistar大鼠制成CLP模型,随机分为手术组和手术 缬沙坦组,每组3,24,72h3个时间点,另8只为假手术对照组,观察心肌损伤指标、RAS和一氧化氮(NO)、丙二醛(MDA)等指标,观察各组各个时间点检测指标的变化。结果CLP术后,手术组血浆肌钙蛋白T(TnT)、脑钠素(BNP)、血浆和组织AngⅡ和NO、MDA浓度在3,24,72h3个时间点均明显升高,而缬沙坦组上述指标较手术未干预组明显好转。结论大鼠发生脓毒症后可出现明显的心肌损伤,表现为TnT和BNP升高。缬沙坦可通过拮抗AT1R抑制RAS过度激活及抑制NO、自由基介导的组织损伤而改善脓毒症心肌损伤。     

丹酚酸B对大鼠缺血心肌组织溶酶体功能的影响

目的探讨丹酚酸B(Sal B)对异丙肾上腺素(ISO)所致大鼠心肌缺血模型心肌溶酶体功能的影响。方法 SD大鼠随机分为空白组,模型组,丹参注射液组和Sal B 12.8、6.4、3.2 mg/kg组。除空白组外,各组大鼠尾静脉注射ISO建立急性心肌缺血模型,连续给药7 d后,PowerLab数据采集分析系统测定各组大鼠心电图变化;试剂盒测定血清中溶酶体相关膜蛋白2(Lamp-2)、组织蛋白酶D(Cat-D)的活性,心脏匀浆中一氧化氮合酶(NOS)、一氧化氮(NO)、Cat-D和溶酶体匀浆中Cat-D的活性;HE染色法检测心肌梗死面积。结果与空白对照组比较(P0.05或P0.01),模型组大鼠心电图T波水平显著升高,血清中Lamp-2、Cat-D的水平显著升高,心脏匀浆中NOS、NO、Cat-D含量升高,溶酶体匀浆中Cat-D含量降低,心肌梗死面积明显增多。Sal B 12.8、6.4 mg/kg组和丹参注射液组能够显著降低心电图T波升高值,降低血清lamp2、Cat-D和心脏匀浆中NOS、NO、Cat-D含量,升高心脏溶酶体匀浆Cat-D含量,与模型组比较(P0.05或P0.01)。结论 Sal B对心肌缺血的保护作用与溶酶体的膜稳定性及水解酶的活性功能有一定的关系。     

左旋卡尼汀对异丙肾上腺素致心肌损害的影响

目的:观察左旋卡尼汀对异丙肾上腺素致心肌损害的保护作用并探讨其机制。方法:采用大鼠皮下注射异丙肾上腺素造成心肌损害模型。心肌切片,HE染色,光镜下观察心肌损害程度;分离心肌线粒体,测定膜脂流动性（LFU）。结果:注射左旋卡尼汀可减轻心肌损害程度;改善线粒体的损伤,改善LFU。结论:左旋卡尼汀能减轻异丙肾对心肌的损害,对线粒体膜脂流动性损伤具有明显的保护作用。     

丙酮酸乙酯对急性坏死性胰腺炎大鼠肺损伤的保护作用

目的:观察丙酮酸乙酯(EP)对急性坏死性胰腺炎(ANP)肺损伤大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和肺组织高迁移率族蛋白B1(HMGB1)mRNA表达的影响,探讨丙酮酸乙酯治疗急性坏死性胰腺炎肺损伤的机制.方法:逆行性胰胆管注射50 g/L牛磺胆酸钠制作ANP模型.随机分成3组,对照组、ANP组和EP治疗组(40 mg/kg,每隔6h静脉注射一次).ELISA法检测血清TNF-α和IL-1β水平;半定量逆转录聚合酶链反应(RT-PCR)法检测肺组织HMGB1 mRNA表达,并观察血氧变化及肺组织的病理变化.结果:ANP组血清TNF-α和IL-1β水平在建模后6h达高峰,12h下降,在此两时点治疗组血清TNF-α和IL-1β水平明显低于ANP组(TNF-α:131.6±29.6 ng/L vs 196.3±16.3 ng/L,65.0±16.6 ng/L vs 90.2±20.1 ng/L,P<0.05;IL-1β:194.9±26.8 ng/L vs 223.0±34.8 ng/L,105.2±24.0 ng/L vs 130.4±23.0 ng/L,P<0.05).ANP组大鼠肺组织HMGB1 mRNA表达水平在ANP后12h明显升高,至24h仍维持在高水平.治疗组肺组织HMGB1 mRNA表达水平在各时间点均明显低于ANP组(0.68±0.11 vs 0.88±0.11,0.81±0.11 vs 1.04±0.10,1.08±0.08 vs 1.33±0.15,P<0.05),且同期肺损伤比ANP组轻.治疗组PaO_2均明显高于ANP组.结论:丙酮酸乙酯能显著抑制TNF-α、IL-1β和HMGB1等早晚期炎症因子,改善低氧血症,对ANP肺损伤有明显保护作用.     

Myocardial ischemic injury induced by isoproterenol in the rabbit: biochemical and chemical alterations

The development of a model of chronic myocardial ischemic injury (MII) in rabbits by administering increasing doses of isoproterenol (ISO) is described. Repeated s.c. injections of increasing doses of ISO (0.5 mg/kg, on day 1 to 15.5 mg/kg, on day 15) resulted in an increase in serum glucose, free fatty acids and creatine phosphokinase. Examination of hearts from ISO-treated rabbits revealed marked hypertrophy of the left ventricle and an increase in total water content. Biochemical analysis showed an increase in left ventricular hydroxyproline and a decrease in ATP and glycogen content following ISO-treatment. Ion measurements revealed extensive accumulation of Na and Ca, with the Ca being preferentially accumulated in the mitochondria. Measurement of subcellular organelle marker enzymes showed decreases in the sarcolemmal Na+-K+-stimulated (ouabain-sensitive), mitochondrial (azide-sensitive) and sarcoplasmic reticulum ATPase activities in the ISO-treated animals. Analysis of lysosomal enzyme activities in myocardial homogenates showed significant decreases in the latency of N-acetyl-beta-glucosaminidase and cathepsin D. The above biochemical alterations in ISO-induced MII generally parallel changes previously seen in the rabbit following acute coronary artery ligation. The present model allows the study of MII uncomplicated by some uncertainties arising from the surgical or anesthetic procedures employed in acute "open-chest" preparations and would permit long-term follow-up studies of pharmacological interventions. The susceptibility of the rabbit to experimental atherosclerosis should allow the development of an experimental model of MII which more closely approximates the clinical situation.     

热水浴对慢性应激心肌损伤的防护作用

目的 观察热水浴对应激性心肌损伤的防护作用。 方法 将18只成年雄性SD大鼠随机分为对照组、应激组和热水浴干预组（简称水浴组），每组6只。利用4 w噪声复合足底电击刺激（4 h/d）构建慢性应激损伤模型；热水浴温度为38~40 ℃。测量大鼠体重、血压和心脏功能，4 w后检测血清应激激素去甲肾上腺素（NE）、血管紧张素（Ang）II和心肌酶肌酸激酶（CK）、乳酸脱氢酶（LDH）水平，免疫荧光和Western blot观察组织蛋白，电镜观察心肌线粒体结构。 结果 与对照组大鼠相比，应激组大鼠存在明显应激反应和心肌损伤，表现为NE、AngII浓度和CK、LDH水平升高（P<0.05）；心肌组织自噬相关蛋白LC3B阳性染色和LC3II/I、p62、Beclin1表达水平增加（P<0.05）；线粒体数量减少并呈现结构紊乱。与应激组大鼠相比，热水浴组大鼠NE、AngII浓度和CK、LDH水平降低，p62和Beclin1水平减少（P<0.05），线粒体结构损伤亦有所逆转。 结论 热水浴能减轻慢性应激状态，调控应激所致心肌细胞自噬紊乱，促进线粒体结构恢复，减轻慢性应激性心肌损伤，其机制有待于进一步研究确认。     

野生山葡萄多酚对异丙肾上腺素诱发的小鼠心肌缺血的保护作用

目的评价野生山葡萄多酚(PVAS)对异丙肾上腺素诱发的小鼠心肌缺血的保护作用。方法采用皮下注射异丙肾上腺素(ISO)建立小鼠急性心肌缺血模型,观察不同剂量PVAS对模型小鼠ECGⅡ导联异常ST段,心肌含水量(MWC),心肌指数(M I)及血清磷酸肌酸激酶(CK)和乳酸脱氢酶(LDH)的影响。结果400 mg/kg PVAS可显著改善ISO诱发小鼠异常ECGⅡ导联ST段抬高,抑制MWC、M I的升高并降低血清CK、LDH水平(P<0.05)。结论PVAS对小鼠急性心肌缺血损伤具有保护作用。     

脂联素对大鼠心肌缺血再灌注损伤的保护作用

目的 观察脂联素对大鼠心肌缺血再灌注损伤的保护作用并探讨其机制.方法 32只8周龄雄性大鼠随机分为假手术组、缺血再灌注组、地尔硫革组和脂联素组,每组8只.(1)假手术组:只穿线,旷置90 min.(2)缺血再灌注组:先阻断血流30 min,再灌注60 min.(3)地尔硫(革)组和脂联素组:先阻断血流30 min,于再灌注开始时,从鼠尾静脉分别注射地尔硫(革)(3.5 μg·g~(-1)min~(-1))或脂联素(60 ng·g~(-1)·min~(-1)),注射2 min,再灌注60 min.各模型组于再灌注60 min后处死大鼠.测定心肌组织一氧化氮(NO),心肌组织半胱氨酸蛋白酶3(Caspase 3)活性,心肌组织腺苷酸活化蛋白激酶(AMPK)活性,过氧化物酶体增殖物激活受体γ(PPARγ)的含量,同时用透射电镜观察大鼠心肌线粒体结构.结果 (1)缺血再灌注组心肌组织中Caspase 3活性显著高于假手术组[(168.50±30.08)μmol/L比(53.25±11.41)μmol/L,P<0.01],AMPK活性、PPARγ含量均显著低于假手术组[(0.74±0.59)IU/ml比(25.63±4.61)IU/ml,P<0.01;0.1894比0.7949,P<0.01],心肌组织中NO含量显著低于假手术组[(6.359±1.355)μmol/L比(10.396±1.901)μmol.L,P<0.01].(2)脂联素组心肌组织中Caspase 3活性显著低于缺血再灌注组[(88.75±6.92)μmol/L比(168.50±30.08)μmol/L,P<0.01],AMPK活性、PPARγ含量均显著高于缺血再灌注组[(27.22 ±4.76)IU/ml比(0.74±0.59)IU/ml,P<0.01;0.8613比0.1894,P<0.01],心肌组织中NO含量显著高于缺血再灌注组[(15.755±1.045)μmol/L比(6.359±1.355)μmol/L,P<0.01].脂联素可保护急性心肌缺血再灌注过程中大鼠心肌细胞线粒体结构的完整性,上述作用优于地尔硫(革).结论 脂联素对缺血再灌注造成的心肌损伤有一定的保护作用,机制可能与其增加心肌细胞AMPK、PPARγ表达,以及抗心肌细胞凋亡作用有关.     

促红细胞生成素对大鼠心肌缺血损伤的保护作用

目的探讨促红细胞生成素(EPO)在大鼠心肌缺血过程中的保护作用及其可能机制。方法建立大鼠心肌缺血模型。将雄性Wistar大鼠60只随机分为治疗组(n=30)和对照组(n=30)。比较24、48 h及1周后血清肌钙蛋白(cTnI)及心肌组织丙二醛(MDA)含量的变化;TFC染色法测定心肌梗死面积;电镜观察心肌超微结构的变化。结果 EPO治疗组大鼠于24、48 h及1周的cTnI水平分别为(10.05±0.81) μg/L、(8.67±0.63) μg/L和(1.36±0.59)μg/L,而对照组相应时间的cTnI水平分别为(11.87±1.19)μg/L、(10.12±0.78)μg/L,和(2.34±0.65)μg/L,差异有统计学意义(P<0.05)。治疗组大鼠心肌组织MDA含量在24、48 h和1周时分别为(1.56±0.09)nmol/L、(1.34±0.18)nmol/L和(1.12±0.10)nmol/L,而对照组心肌组织存相对应时间的MI)A含量分别为(2.02±0.14)nmol/L、(1.84±0.20)nmol/L和(1.61±0.11)nmol/L,差异有统计学意义(P<0.05)。EPO治疗组大鼠于24、48 h及1周的心肌梗死面积(心肌梗死面积/心室肌总面积)分别为30.33%±2.02%、26.25%±3.81%和27.18%±5.15%,而对照组相应时间的心肌梗死面积比例分别为41.11%±1.65%、36.25%±1.85%和38.58%±3.09%,治疗组的心肌梗死面积明显减小,与对照组相比,差异有统计学意义(P均<0.05)。结论 EPO对大鼠心肌急性缺血损伤有明显的保护作用,其机制可能与减轻氧自由基及钙超载损害有关。     

虾青素对异丙肾上腺素诱导的大鼠心肌纤维化的影响

目的 探讨虾青素对异丙肾上腺素（ISO）诱导的大鼠心肌纤维化的影响。方法 SD大鼠腹腔注射异丙肾上腺素（5mg/kg/d），连续注射14d，建立心肌纤维化模型，从造模第二天开始给予虾青素（5mg/kg/d和10mg/kg/d）灌胃，连续21天。实验结束后超声心动图检测大鼠心脏功能，计算心脏指数，Masson染色观察心肌纤维化水平，Western blotting 方法检测心肌胶原Ⅲ、转化生长因子-β1（TGF-β1）蛋白的表达。结果 与正常对照组比较，模型组左心室射血分数（EF）和左心室短轴缩短分数（FS）明显降低（P<0.05）,心脏指数增加，心肌纤维化明显，胶原蛋白Ⅲ及TGF-β1表达水平增加（P<0.05）；与模型组比较，低剂量虾青素组和高剂量虾青素组EF和FS明显升高（P<0.05），心脏指数减低（P<0.05），心肌纤维化程度减低，心肌胶原蛋白Ⅲ、TGF-β1表达水平明显降低（P<0.05）。 结论 虾青素能够降低异丙肾上腺素诱导的心肌纤维化水平，改善心功能。     

Protective effect of acupuncture preconditioning on oxidative stress injury induced by myocardial ischemia-reperfusion injury in rats

正Objective To observe the protective effect of acupuncture preconditioning at"Jiaji"(EX-B 2)on acute myocardial ischemia-reperfusion injury(MIRI)in the rats and explore the mechanism.Methods Fifty Wistar rats were randomly divided into a control group,a model group,a Jiaji group,a Neiguan group and a Quchi group,10 rats in each one.In the Jiaji group,the     

安石榴苷减轻心肌缺血/再灌注损伤的作用及机制研究

目的 探讨安石榴甙（PUN）预先处理对心肌缺血/再灌注损伤（MI/RI）的作用及其机制。 方法 选取成年雄性SD大鼠,PUN 30 mg/（kg·d）生理盐水灌胃7 d后,建立心肌缺血再灌注（MI/R）模型。采用右侧颈总动脉插管检测心脏功能,用伊文思蓝和氯化三苯基四氮唑（TTC）双染检测心梗面积,测定血清肌酸激酶同工酶（CK-MB）和乳酸脱氢酶（LDH）活性反映心肌损伤,原位末端标记（TUNEL）法检测心肌细胞凋亡,比色法检测心肌丙二醛（MDA）含量和超氧化物歧化酶（SOD）的活性,蛋白免疫印迹检测磷酸腺苷活化蛋白激酶（AMPK）表达及磷酸化。 结果 PUN预先处理可改善MI/R后的心脏功能,减少心梗面积和心肌细胞凋亡,降低CK-MB和LDH的活性,降低心肌氧化应激,增加AMPK磷酸化（均P<0.05或P<0.01）,而使用AMPK抑制剂（compound c）可阻断PUN对MI/R的保护作用（P<0.05或P<0.01）。 结论 PUN预先处理可减轻MI/RI,其机制可能与其激活AMPK有关。     

N-乙酰半胱氨酸对大鼠肺缺血再灌注损伤的保护作用

目的探讨N-乙酰半胱氨酸(NAC)对大鼠在体肺缺血再灌注(I/R)损伤的保护作用。方法建立大鼠在体肺缺血再灌注模型,将30只SD大鼠随机分成假手术对照组,缺血再灌注组(I/R组)和N-乙酰半胱氨酸组(NAC组),NAC组缺血前1 h给予腹腔注射N-乙酰半胱氨酸200 mg/kg。再灌注2 h后摘取左肺,分别对各组进行以下检测:肺湿/干比(W/D)、超氧化物歧化酶(SOD)活力、髓过氧化物酶(MPO)活性、丙二醛(MDA)含量并进行病理学检查及肺组织损伤定量评价(IQA)。结果I/R组肺W/D和IQA显著高于假手术组(P0.01),NAC组上述指标明显降低(P0.01)。病理学结果显示三组动物肺组织结构基本正常,假手术组无充血;与NAC组比较,I/R组肺组织充血明显、白细胞浸润更严重及肺间质高度淤血水肿。I/R组MDA含量和MPO活性较假手术组明显升高(P0.01),SOD活性显著下降(P0.01)。NAC能明显减少MDA含量和降低MPO活性,提高SOD活性(P0.01)。结论N-乙酰半胱氨酸对肺缺血再灌注损伤具有保护作用,可能与其抗氧化作用和抑制中性粒细胞激活有关。     

Protective effects of trimetazidine against vascular endothelial cell injury induced by oxidation

Objective To explore the protective effects of trimetazidine on vascular endothelial cells injury induced by hydrogen peroxide (H2O2) and its pharmacological mechanisms of anti-oxidation. Methods Human umbilical vein endothelial cells (HUVECs) were injured by H2O2. Next, the cells were treated with three different concentrations of trimetazidine (1μmol/L,10μmol/L,100μmol/L, respectively). The viability of cells was detected by methyl thiazoeyl tetrazolium (MTT) assay. In addition, malondialdehyde (MDA) contents, superoxide dismutase (SOD) and secretion of NO were measured. Results Trimetazidine could enhance the viability of the injured HUVECs induced by oxidation, decrease the level of MDA, enhance the SOD activity, and increase the secretion of nitrogen monoxide. These effects were in a certain dose-dependent manner and the difference was significant among the three concentrations (P<0.05). Conclusions Our results suggest that trimetazidine may protect lipid peroxidation and prevent oxidation-induced cellular dysfunction of HUVECs.     

卡维地洛和庚醇对心肌缺血再灌注损伤的保护作用

目的研究卡维地洛（CVD）、庚醇（HT）在缺血再灌注心肌损伤中作用。方法通过建立的心脏缺血再灌注模型，采用2％氯化三苯四唑（TTC）染色测量心肌梗死的重量，监测心肌型肌酸激酶同功酶（CK—MB）、乳酸脱氢酶（LDH）、丙二醛（MDA）和一氧化氮（NO）等的变化。观察CVD、HT对心肌梗死的影响。结果在缺血30min，再灌注6h后，CVD减少CK—MB、LDH及MDA的释放，稳定NO的分泌。HT组在一定程度上也减少了LDH、CK—MB的释放，但对NO、MDA的释放似乎没有太大影响。CVD组的大鼠梗死心肌仅占左心室心肌重量的（6．2±1.1）％，比对照组减少了51.6％。HT组梗死心肌占左心室心肌重量的（7．4±1.0）％，比对照组减少了42．2％。HE常规染色发现CVD组心肌细胞损伤程度明显减轻，粒细胞浸润也明显减少，大部分仅表现肌纤维肿胀和断裂。CVD可以防止内皮型一氧化氮合酶的减少。电镜下，CVD组和HT组心肌润盘肌丝、线粒体等损伤较轻。结论CVD通过B受体拮抗、抗氧化等方面的作用来保护心肌。HT可能是使缝隙连接可逆性解藕联产生心肌保护作用。     

Protective action of omeprazole against gastric mucosal injury induced by hemorrhagic shock in rats

The efficacy of omeprazole in preventing gastric mucosal injury induced by hemorrhagic shock in rats and the putative mechanisms involved in this effect were investigated in the present study. Omeprazole did not affect mean arterial blood pressure under both basal conditions and induction of hemorrhagic shock, but it evoked a marked increase in Alcian blue recovery from gastric preepithelial mucus. The morphometric analysis of histological sections revealed that omeprazole caused a significant reduction of hemorrhagic shock-induced damage of gastric mucosa. Ranitidine, used as the reference drug, failed to affect mean arterial blood pressure, Alcian blue recovery from gastric mucus, or hemorrhagic shock-induced damage of gastric mucosa. Both omeprazole and ranitidine exerted a significant inhibition of gastric acid output from anesthetized pylorus-ligated rats. Overall, the present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by hemorrhagic shock and suggest that an enhancement of gastric mucus secretion contributes to this protective action.     

生黄合剂对大鼠心肌缺血再灌注损伤的保护作用

目的观察生黄合剂对大鼠心肌缺血再灌注损伤(MIRI)的保护作用。方法将48只SD大鼠随机分为6组,即空白对照组、模型组、阳性药物组及生黄合剂低、中、高剂量组,每组8只,分别给药7 d后,建立MIRI模型。检测大鼠血清乳酸脱氢酶(LDH)及心肌丙二醛(MDA)和超氧化物歧化酶(SOD)的含量,用TUNEL法检测心肌细胞凋亡情况,并观察心肌组织形态学改变。结果与模型组比较,生黄合剂能降低大鼠LDH及MDA的含量,增加SOD活性,降低心肌细胞凋亡指数,改善心肌组织病理损害。结论生黄合剂对大鼠MIRI具有保护作用,其机制可能为通过抗自由基作用来抑制MIRI诱导的细胞凋亡。