大豆磷脂脂质体对缺血—再灌注心肌细胞超微结构的影响

利用Langendroff's离体心脏灌流和心肌细胞培养缺—血再灌注模型,探讨大豆磷脂脂质体对心肌细胞超微结构的影响。结果表明:缺血—再灌注将导致心肌细胞膜和线粒体超微结构的损害;大豆磷脂脂质体可保护心肌细胞膜和线粒体膜的完整,抑制线粒体的水肿,嵴及基质密度的降低等。其作用机理可能与脂质体和细胞膜间的相互作用有关。     

高渗液预灌注增强高血压大鼠心脏抗氧化及抗缺血能力

目的本实验以高渗透压平衡灌注液对正常大鼠和自发性高血压大鼠的离体心脏进行预灌注,观察其对心肌缺血再灌注损伤后心功能的影响,并通过测定心脏组织抗氧化物质的变化探讨其机理。方法采用Langendorff离体心脏灌注模型,大鼠心脏用氯化钠加入Krebs-Henseleit平衡灌注液中形成高渗平衡灌注液(400mOsm/L)预灌注心脏20min,全心热缺血40min,然后以正常渗透压平衡灌注液复灌40min,监测灌注过程中心功能变化,并测定抗氧化酶的活性及心肌抗氧化物的含量。结果预先用高渗平衡灌注液处理高血压大鼠和正常大鼠心脏与未处理相比,缺血再灌注后的冠脉流出液增加,冠脉阻力减小,心率与左室发展压乘积增加,左室压力上升及下降最大速度提高。心肌组织肌酸激酶的漏出量和丙二醛的含量均显著减少(P<0.01),超氧化物歧化酶和过氧化氢酶的活性增加(P<0.01)。高渗处理尚可以增加心肌过氧化氢酶及血红素加氧酶含量。结论高渗透压预灌注可以改善高血压大鼠和正常大鼠的离体心脏缺血再灌注的心肌细胞及心功能损伤,该作用可能与高渗透压增加心肌组织的抗氧化能力有关。     

高渗液预灌注增强高血压大鼠心脏抗氧化及抗缺血能力

目的本实验以高渗透压平衡灌注液对正常大鼠和自发性高血压大鼠的离体心脏进行预灌注,观察其对心肌缺血再灌注损伤后心功能的影响,并通过测定心脏组织抗氧化物质的变化探讨其机理.方法采用Langendorff离体心脏灌注模型,大鼠心脏用氯化钠加入Krebs-Henseleit平衡灌注液中形成高渗平衡灌注液( 400 mOsm/L )预灌注心脏20 min,全心热缺血40 min,然后以正常渗透压平衡灌注液复灌40 min,监测灌注过程中心功能变化,并测定抗氧化酶的活性及心肌抗氧化物的含量.结果预先用高渗平衡灌注液处理高血压大鼠和正常大鼠心脏与未处理相比,缺血再灌注后的冠脉流出液增加,冠脉阻力减小,心率与左室发展压乘积增加,左室压力上升及下降最大速度提高.心肌组织肌酸激酶的漏出量和丙二醛的含量均显著减少(P<0.01),超氧化物歧化酶和过氧化氢酶的活性增加(P<0.01).高渗处理尚可以增加心肌过氧化氢酶及血红素加氧酶含量.结论高渗透压预灌注可以改善高血压大鼠和正常大鼠的离体心脏缺血再灌注的心肌细胞及心功能损伤,该作用可能与高渗透压增加心肌组织的抗氧化能力有关.     

预处理对心肌细胞的保护作用

为探讨缺氧和缺血预处理对心肌细胞的保护作用,分别在培养的乳鼠心肌细胞缺氧／复氧模型、离体大鼠灌注和在体大鼠心肌缺血／再灌注模型中,观察缺血和缺氧预处理对心肌细胞再次长时间缺氧／复氧或缺血／再灌注损伤的保护作用,结果发现,在培养原乳鼠心肌细胞中,缺氧预处理组细胞存活率和超氧化物歧化酶含量较缺氧／复氧组增加（Ｐ〈０．０１）,乳酸脱氢酶的释放和丙二醛含量则减少（Ｐ〈０．０１）。对离体或在体大鼠心脏的缺血     

大剂量当归预适应抗心肌缺血再灌注后心肌细胞凋亡的机制

目的观察大剂量当归水煎液预适应对缺血再灌注(IR)大鼠心肌细胞凋亡及心肌组织Bcl-2及Bax蛋白表达的影响。方法应用离体灌流大鼠心脏,复制大鼠心肌IR与缺血预适应(IPC)模型,并以不同大剂量当归水煎液灌胃6 w后,取大鼠心脏进行离体灌注,复制当归IPC模型,以TTC法测定心肌梗死面积,以Tunel法检测细胞凋亡,Western印迹法检测Bcl-2及Bax蛋白表达。结果大剂量当归水煎液预适应能有效降低IR大鼠心肌梗死面积,降低心肌细胞的凋亡率,并增加心肌组织Bcl-2的表达而抑制Bax的表达,且呈现明显剂量-效应关系(P0.05,P0.01)。结论大剂量当归水煎液预适应可增加心肌组织Bcl-2的表达而抑制Bax的表达,从而减少IR大鼠心肌细胞的凋亡,对IR大鼠心肌具有明显保护作用。     

腺苷对大鼠离体心脏功能及心肌细胞凋亡的影响

目的 探讨腺苷预处理对离体灌流大鼠心脏功能及心肌细胞凋亡的影响.方法 将30只雄性Wistar大鼠随机分为对照组、缺血—再灌注（IR）组、腺苷组,各10只.采用戊巴比妥钠腹腔注射麻醉,同时腹腔注射肝素,麻醉后开胸暴露心脏,快速取出心脏.用Langehdorff离体灌注大鼠心脏K-H液,腺苷组、IR组建立心肌缺血—再灌注损伤模型.对照组灌注时间为120 min;IR组灌注K-H液30min,缺血30 min,K-H液60 min;腺苷组灌注K-H液10 min,给予腺苷20 min,缺血30 min,K-H液60 min.记录实验初始和结束时左室发展压（LVDP）和平均冠脉流量（CSF）,测定心肌组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性,TUNEL方法检测细胞凋亡.结果 IR组和腺苷组实验结束时LVDP、CSF低于实验初始（P均＜0.01）;实验结束时腺苷组、对照组的CSF均高于IR组,LVDP水平IR组＜腺苷组＜对照组,P均＜0.05.大鼠心肌组织中MDA水平IR组＞腺苷组＞对照组,P均＜0.01,腺苷组及对照组心肌组织SOD活性高于IR组,P均＜0.01.心肌细胞凋亡率IR组＞腺苷组＞对照组P＜0.01.结论 腺苷预处理能改善离体灌流大鼠心功能,其机制可能与减轻缺血-再灌注损伤和抑制心肌细胞凋亡有关.     

七氟醚后处理对大鼠离体心肌缺血/再灌注时线粒体融合蛋白2表达及细胞凋亡的影响

目的探讨七氟醚后处理对大鼠离体心肌缺血/再灌注时线粒体融合蛋白2（Mfn2）表达及细胞凋亡的影响。方法健康成年雄性SD大鼠,体重220g~280g,采用随机数字表法,将其分为假手术组（S组）、缺血/再灌注组（I/R组）、七氟醚后处理组（Sev组）。采用Langendorff离体心脏灌流系统建立心肌缺血/再灌注损伤模型。K-H液平衡灌注30min后,S组继续灌注K-H液150min;I/R组停灌30min,复灌120min;Sev组停灌30min后灌注含3%七氟醚饱和的K-H液5min,再用K-H液冲洗10min,继续灌注K-H液,总灌注时间为120min。于再灌注结束时取心肌组织,采用免疫组化法测定Mfn2蛋白表达,TUNEL法测定心肌细胞凋亡,计算心肌细胞凋亡指数（AI）。电镜下观察心肌细胞及线粒体的超微结构。结果与S组比较,I/R组和Sev组Mfn2蛋白表达下调,AI增加（P〈0.05）;与I/R组比较,Sev组Mfn2蛋白表达上调,AI降低（P〈0.05）。电镜结果显示I/R组心肌细胞线粒体出现较重损伤,线粒体膜断裂,嵴不规则或消失。Sev组心肌细胞线粒体损伤较轻,线粒体形态完整。结论七氟醚后处理对大鼠离体心肌缺血/再灌注损伤具有保护作用,其机制可能与上调心肌组织Mfn2表达,保护线粒体形态完整,减少心肌细胞凋亡有关。     

腐胺对大鼠心肌缺血再灌注损伤的保护作用

目的 :观察腐胺对大鼠心肌缺血再灌注损伤的保护作用。方法 :利用 Langendroff- Neely离体心灌注方法 ,以缺血 12 0 min,再灌注 2 0 min制备大鼠心肌缺血再灌注损伤模型。对照组 (n=12 ) ,采用St.Thomas液作为心停搏液。实验组 (n=12 )以腐胺 10 mg/ ml作为心停搏液 (St.Thomas液 )的添加剂。测定心脏停搏前和缺血 12 0 min,再灌注 2 0 min后的心率、主动脉流量、冠脉流量和心输出量。测定心脏缺血 12 0 min,再灌注 2 0 min后心肌组织 MDA、SOD,并进行心肌超微结构比较研究。结果 :实验组较对照组心功能改善 ,缺血再灌注损伤心肌 SOD活性无明显变化 ,明显降低缺血再灌注损伤心肌MDA水平 ,减轻细胞膜结构的损害 ,心肌水肿程度明显减轻 ,心肌结构保存好。结论 :腐胺对大鼠心肌缺血再灌注损伤具有保护作用     

西洋参茎叶三醇组皂苷对离体缺血再灌注损伤心肌的影响

目的 探讨西洋参茎叶三醇组皂苷(PQTS)对大鼠离体缺血再灌注损伤心肌AST、CPK、LDH及冠脉流量的影响。方法 采用大鼠离体心脏Langendorff灌流模型，观察PQTS对缺血再灌注损伤心肌冠脉流量及冠脉流出液中AST、CPK、LDH释放量的影响。结果与缺血再灌注组比较，PQTS(30、100、300μg／ml)可以不同程度地降低冠脉流出液中的AST、CPK、LDH的释放，并提高再灌注期间的冠脉流量。结论 PQTS对大鼠离体缺血再灌注损伤心肌具有一定的保护作用。     

减阻剂减轻大鼠离体心脏缺血/再灌注损伤的作用

目的 应用减阻剂聚氧化乙烯（polyethylene oxide,PEO）减轻大鼠离体心脏缺血/再灌注（I/R）损伤的作用。方法 Wistar大鼠50只随机分为5组,制备Langendorff离体心脏I/R模型,分为对照组、I/R组、缺血-低剂量PEO再灌注组（低剂量组）、缺血-中剂量PEO再灌注组（中剂量组）、缺血-高剂量PEO再灌注组（高剂量组）。通过多导生理记录仪记录灌注心脏的左心室最大收缩压峰值（LVPSP）、左室舒张末压峰值（LVEDP）、左室内压等容相最大上升及下降速率（+dp/dtmax,-dp/dtmax）、心率、冠脉流量。检测冠脉流出液的乳酸脱氢酶（lactate dehydrogenase,LDH）的含量。结果 再灌注30 min及60 min后,中剂量及高剂量的PEO对I/R心肌的LVPSP、LVEDP、+dp/dtmax、-dp/dtmax均有明显改善作用（P<0.05）。中剂量及高剂量PEO在维持离体心脏的心率方面优于低剂量组和I/R组（P<0.05）,冠脉流出液的容积增加（P<0.05）。应用中剂量及高剂量的PEO灌注后,冠脉流出液中LDH含量明显下降（P<0.05）。结论 PEO作为减阻剂,减低Langendorff离体心脏I/R系统的流体阻力,改善离体心脏的收缩及舒张功能,增加冠脉流出液量,减少心肌细胞损伤,抑制心肌细胞凋亡,对心肌I/R损伤的治疗提供新的研究思路。     

川芎嗪、缬沙坦及曲美他嗪对乳鼠肥大心肌细胞线粒体结构和能量代谢的影响

目的通过大鼠原代心肌细胞培养,探讨心肌肥大过程中有关心肌细胞线粒体结构和功能的病理改变以及川芎嗪、缬沙坦和曲美他嗪对其的药理作用。方法分离和培养大鼠原代心肌细胞,并与血管紧张素Ⅱ(AngⅡ)共培养72h、96h。BCA法检测细胞总蛋白含量,倒置显微镜拍摄并测量细胞直径,反映心肌细胞增殖情况;荧光显微镜测量线粒体内膜膜电位(ΔΨm)、酶标仪检测线粒体单胺氧化酶(MAO)活性、分光光度计检测线粒体细胞色素C氧化酶(COX)活性和线粒体损伤百分率,高效液相色谱法检测心肌细胞内ATP、ADP、AMP含量,反映心肌细胞线粒体结构和功能的损伤情况。在此基础上给予川芎嗪、缬沙坦和曲美他嗪,观察对心肌细胞重构中线粒体结构和功能的药理作用。结果在细胞肥大过程中,心肌细胞MAO活性和线粒体外膜损伤百分率均显著升高(P<0.01),线粒体COX活性和线粒体ΔΨm均显著减低(P<0.01),ATP、ADP含量显著减少(P<0.01),AMP含量显著增加(P<0.01)。川芎嗪能抑制AngⅡ引起的心肌细胞蛋白质合成增加和细胞直径增大,改善线粒体外膜损伤,提高线粒体内膜膜电位及COX活性,降低MAO活性(72h时P<0.01,96h时P<0.05),增加ATP、ADP含量、降低AMP含量。缬沙坦能抑制AngⅡ引起的心肌细胞蛋白质合成增加和细胞直径增大,改善线粒体外膜损伤,提高线粒体内膜膜电位(P<0.05)及MAO活性(72h时P<0.01,96h时P<0.05),增加ATP、ADP含量、降低AMP含量(P<0.01)。曲美他嗪能在72h升高线粒体膜电位(P<0.05),增加ATP、ADP含量(P<0.05)。结论在心肌肥大过程中,存在线粒体结构和功能损害。川芎嗪和缬沙坦在逆转心肌细胞肥大过程中具有保护心肌细胞线粒体结构和功能的作用,曲美他嗪无显著逆转心肌细胞重构作用,对能量代谢的改善作用亦有限。     

Oxidative injury to myocardial membrane: direct modulation by endogenous alpha-tocopherol

Peroxidation of myocardial-membrane phospholipid is considered an important pathogenic component of heart muscle damage in ischemia and reperfusion. The extent to which membrane alpha-tocopherol (vitamin E) in the heart can modulate such damage and protect against it is a matter of controversy. The relative alpha-tocopherol deficit of spontaneously-hypertensive (SH) rat myocardium as compared to the myocardium of the Wistar-Kyoto (W/K) normotensive parent strain prompted use of these animals to identify and characterize any protective antiperoxidant role of endogenous, myocardial-membrane alpha-tocopherol. With exposure to a superoxide- and iron-containing initiator of peroxidation, the membrane complements from the ventricular myocardia of the SH rat and the W/K parent strain were found to have very different peroxidative-injury profiles. SH-rat myocardial membrane demonstrated a marked sensitivity to peroxidation as reflected in the acute onset and rapid progression of phospholipid damage. The greater susceptibility of SH-rat myocardial membrane to free-radical attack could not be explained by inter-strain compositional differences in membrane polyunsaturated fatty acids or fatty aldehydes. Rather, the basis for the enhanced peroxidation was identified as the 3-fold lower alpha-tocopherol content of SH-rat myocardial membrane with respect to the heart-muscle membrane from the normotensive animal. The relative alpha-tocopherol deficit not only increased the susceptibility of SH-rat cardiac membrane to damage under pro-oxidant conditions, but also reduced the efficacy of exogenously supplied antioxidant intervention. These findings demonstrate that membrane alpha-tocopherol tone is a critical protectant of myocardial phospholipid against oxidative injury and acts as a determinant of the course of heart-membrane peroxidative damage.     

Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart: involvement of reactive oxygen species and cardiolipin

Reactive oxygen species (ROS) are considered an important factor in ischemia/reperfusion injury to cardiac myocytes. Mitochondrial respiration is an important source of ROS production and hence a potential contributor to cardiac reperfusion injury. In this study, we have examined the effect of ischemia and ischemia followed by reperfusion of rat hearts on various parameters related to mitochondrial function, such as complex I activity, oxygen consumption, ROS production, and cardiolipin content. The activity of complex I was reduced by 25% and 48% in mitochondria isolated from ischemic and reperfused rat heart, respectively, compared with the controls. These changes in complex I activity were associated with parallel changes in state 3 respiration. The capacity of mitochondria to produce H2O2 increased on reperfusion. The mitochondrial content of cardiolipin, which is required for optimal activity of complex I, decreased by 28% and 50% as function of ischemia and reperfusion, respectively. The lower complex I activity in mitochondria from reperfused rat heart could be completely restored to the level of normal heart by exogenous added cardiolipin. This effect of cardiolipin could not be replaced by other phospholipids nor by peroxidized cardiolipin. It is proposed that the defect in complex I activity in ischemic/reperfused rat heart could be ascribed to a ROS-induced cardiolipin damage. These findings may provide an explanation for some of the factors responsible for myocardial reperfusion injury.     

Preservation of membrane phospholipids by propranolol, pindolol, and metoprolol: a novel mechanism of action of beta-blockers.

In this study, we examined the effects of three different beta-blockers, propranolol, pindolol, and metoprolol, on membrane phospholipid preservation in the ischemic and reperfused rat heart. Isolated rat hearts were perfused with Krebs-Henseleit bicarbonate buffer by the Langdendorff technique in the presence or absence of propranolol, pindolol, or metroprolol (20 microM each) for 15 mins at 37 degrees C. Hearts where then either made ischemic alone at 37 degrees C for 30 mins, or followed by 30 mins of reperfusion. Coronary flow and perfusate creatine kinase content were monitored during both pre- and post-ischemic periods. At the end of the experiment, hearts were frozen by freeze-clamping at liquid nitrogen temperature. Membrane phospholipids, fatty acid composition of these phospholipids, non-esterified free fatty acids, and myocardial thiobabituric acid (TBA) reactive product were examined in these hearts. The beta-blocker-treated hearts exhibited significantly less lipid peroxidation than the control hearts (P less than 0.05), as indicated by decreased formation of TBA reactive product and the higher percentage of unsaturated fatty acids in the phosphatidylcholine (PC) in heart. In addition, compared to the control group, less accumulation of free fatty acids was observed in the propranolol and pindolol treated groups. Finally, reduced myocardial creatine kinase release and enhanced recovery of coronary flow indicated significant myocardial preservation by these beta-blockers. The efficacy of these beta-blockers were in the following order: propranolol, pindolol, metoprolol. These results suggest that beta-blockers could also protect an ischemic heart from reperfusion injury by preserving the membrane phospholipids.     

Effects of N-(2-mercaptopropionyl)-glycine on mitochondrial function in ischemic-reperfused heart

OBJECTIVE: A possible mechanism for N-(2-mercaptopropionyl)-glycine (MPG) underlying the improvement of contractile function and mitochondrial activity of ischemic-reperfused rat hearts was examined. METHODS: Isolated, perfused hearts were subjected to 35 min ischemia-60 min reperfusion. At the end of ischemia or reperfusion, myocardial Na(+) content and mitochondrial oxygen consumption rate (OCR) were examined. The perfused heart was treated with 0.1-1 mM MPG for 30 min prior to ischemia or for the first 30 min of reperfusion. RESULTS: Ischemia increased myocardial Na(+) content (sodium overload) and decreased mitochondrial OCR. The left ventricular developed pressure (LVDP) of the untreated heart recovered to 19.8+/-3.8% of the preischemic value and the infarct area amounted to 23.3+/-1.7% of the left ventricle. The thiobarbiturate-reacting substance (TRS) was also increased in the reperfused, but not ischemic, myocardium. Pretreatment of the perfused heart with 0.3-1 mM MPG attenuated the ischemia-induced sodium overload and decrease in the OCR. Pretreatment with the agent also enhanced the postischemic recovery of LVDP, attenuated reperfusion-induced increase in TRS, and reduced the infarct area. Although the postischemic treatment with MPG suppressed the increase in TRS in the reperfused myocardium, a LVDP recovery of reperfused hearts was not observed. Cardiac mitochondria were isolated and examined for the direct effect of MPG on their function. Incubation with either 12.5 mM sodium lactate or 1 microM phenylarsine oxide neither altered the mitochondrial membrane potential nor induced mitochondrial swelling, whereas incubation with a combination of these agents elicited the membrane potential depolarization and swelling. Incubation of mitochondria with 1 mM MPG attenuated these events. CONCLUSION: These results suggest that both attenuation of sodium overload and preservation of the mitochondrial function may largely contribute to cardioprotection of MPG in the ischemic-reperfused heart.     

Dissociation between contractile function and oxidative metabolism in postischemic myocardium. Attenuation by ruthenium red administered during reperfusion.

The oxidative metabolic rate may be disproportionately high compared with contractile function in postischemic reperfused myocardium. To study the potential involvement of intracellular calcium transport in high energy expenditure after reperfusion, we determined in isolated rat hearts the effect of ruthenium red, an inhibitor of mitochondrial calcium transport, on recovery of contractile function and oxidative metabolic rate. Hearts subjected to 60 minutes of no-flow ischemia exhibited, at 15 minutes after the onset of reperfusion, poor recovery of left ventricular pressure development to only 7% of the corresponding value measured in control hearts (p less than 0.01). However, myocardial oxygen consumption was recovered to 84% of control (p = NS). The ratio of isovolumic contractile performance (expressed as the product of heart rate and left ventricular pressure development) to myocardial oxygen consumption was severely depressed to 6% of control (p less than 0.01). Supplementation of the perfusate with 6 microM ruthenium red during the initial 40 minutes of reperfusion resulted in a reduction of myocardial oxygen consumption to 65% of the value measured after 15 minutes of reperfusion in hearts reperfused without ruthenium red (p less than 0.01), despite a threefold increase of left ventricular pressure development (p less than 0.05). Oxidation of both palmitate and glucose was reduced to a comparable extent by ruthenium red. The ratio of contractile performance to myocardial oxygen consumption increased progressively during infusion of ruthenium red and did not differ further from control hearts after 30 minutes of reperfusion. Cumulative myocardial release of creatine kinase was reduced by 47% (p less than 0.05) in hearts reperfused with ruthenium red-containing medium. The results provide circumstantial evidence for the hypothesis suggesting that enhanced energy expenditure by intracellular calcium transport may be involved in the mechanisms underlying the dissociation between left ventricular performance and myocardial oxidative metabolic rate early after postischemic reperfusion.     

Mitochondrial damage during ischemia determines post-ischemic contractile dysfunction in perfused rat heart

Possible mechanisms underlying sodium overload-induced ischemia/reperfusion injury in perfused rat hearts were examined. Massive accumulation of myocardial Na(+) occurred during ischemia, suggesting cytosolic sodium overload in cardiac cells. Treatment of the pre-ischemic heart with 0.3 micromol/l tetrodotoxin or 3 micromol/l ethyl-isopropyl amiloride enhanced post-ischemic contractile recovery (72 or 82% of initial vs 24% for untreated group), which was associated with suppression of tissue Na(+) accumulation (138 or 141% of initial vs 270% for untreated group), restoration of tissue high-energy phosphates, and preservation of the ability of mitochondria to produce ATP in the ischemic/reperfused heart. The release of cytochrome c from the ischemic heart was observed, which was blocked by treatment of the pre-ischemic heart with these agents. The improvement of post-ischemic contractile recovery by these agents was closely correlated with the ability of mitochondria to produce ATP during ischemia. To examine the effects of sodium overload on mitochondrial function, isolated mitochondria were incubated in the presence of various concentrations of Na(+). Na(+) induced mitochondrial membrane perturbations such as depolarization of the membrane potential, mitochondrial swelling, cytochrome c release from isolated mitochondria, and a reduction in oxidative phosphorylation. These events in the isolated mitochondria were not blocked by the presence of the above agents. The results suggest that cytosolic sodium overload in cardiac cells may induce deterioration of the mitochondrial function during ischemia and that this mitochondrial damage may determine post-ischemic contractile dysfunction in perfused rat hearts.     

Perilipin 5缺失导致线粒体功能异常加剧肥胖小鼠心肌的氧化应激损伤

目的 探讨Perilipin 5缺失是否会导致小鼠的线粒体功能异常,从而加剧肥胖小鼠心肌的氧化应激损伤。 方法 对各组小鼠心脏进行超声分析,对心肌组织进行HE染色观察心肌肥厚程度,检测心肌组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）水平,Western blot检测心肌组织线粒体以及胞质内 Cytochrome C蛋白的表达水平。 结果 与ob/ob小鼠对比,ob/ob/Plin5-/-小鼠心脏LVEF、LVIDd进一步降低（均P<0.05）,LVIDs进一步增大（P<0.01）,心肌细胞横截面积（P<0.05）和LVPWd进一步增大（P<0.05）,MDA进一步上升（P<0.01）,SOD进一步下降（P<0.05）,心肌线粒体 Cytochrome C蛋白表达明显降低（P<0.01）,胞质中 Cytochrome C蛋白表达明显升高（P<0.01）。 结论 Plin5的缺失可能通过干扰线粒体功能,加剧肥胖小鼠心肌的氧化应激损伤,进而引起小鼠心脏功能的进一步损害。