Cardioprotective effect of hydroalcoholic extract of Tecoma stans flowers against isoproterenol induced myocardial infarction in rats

ObjectiveTo investigate the cardioprotective effect of 70% ethanolic extract of Tecoma stans (T. stans) flowers against isoproterenol-induced myocardial infarction in rat myocardium.MethodsWister rats were pretreated with 70% ethanolic extract of T. stans flowers (250 and 500 mg/kg) orally for 14 d and then intoxicated with isoproterenol [200 mg/(kg · day), s.c.] for 2 consecutive d. The biochemical markers for myocardial infarction such as alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, creatinine kinase, total cholesterol, triglycerides, low density lipoproteins and high density lipoproteins were determined. In addition the antioxidant status on heart tissue is also evaluated by testing the activities of antioxidant enzymes such as lipid peroxidation, superoxide dismutase, reduced glutathione and catalase.ResultsThe results indicated that pretreatment with 70% ethanolic extract of T. stans flowers prevented fall in antioxidants and retarded elevation of cardiac damage markers in isoproterenol treated rats, significantly. In addition, these findings were evidently supported by the remarkable protection revealed in the histopathological studies, even GC-MS analysis data also substantiated out investigation.ConclusionsIt was concluded that, in addition to poly phenolics, some of the phyto fragments found during GC-MS analysis might also contributed to the cardiac protection offered by the extract.     

A novel phytochemical, digoxigenin-3-O-rutin in the amelioration of isoproterenol-induced myocardial infarction in rat: a comparison with digoxin

Introduction: The commonly used cardiac glycoside, digoxin (DIG), has a narrow therapeutic window. Although some investigations were made to counteract its toxic effects, no alternate phytochemical is available till date that is more potent and safer than DIG. Aims : Our main aim was to isolate a novel cardenolide from the seeds of Trigonella foenum graceium and to evaluate its relative potential in comparison to that of DIG. Experimental design: In one experiment effects of the isolated compound at 2.5, 5.0, and 10 mg/kg (p.o.) were evaluated in isoproterenol (ISO)‐induced cardiovascular problems in rats. As the test drug (TDR) reversed most of the ISO‐induced changes, it was subjected to the phytochemical analyses and was identified as digoxigenin‐3‐O‐rutin. In another experiment effects of DIG and rutin (Rtn) were compared with those of TDR or DIG alone. The hydroxyl radical scavenging activity was also measured by electron spin resonance (EPR). Results: digoxigenin‐3‐O‐rutin at 10 mg/kg markedly reduced the ISO‐induced increase in cardiac lipid peroxidation and in the levels of serum creatinine phosphokinase‐MB, glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, and creatinine. It also reversed the ISO‐induced changes in the cardiac histomorphology. Interestingly TDR appeared to be more effective than DIG alone or DIG and Rtn in combination. Conclusion: The newly isolated digoxigenin‐3‐O‐rutin appears to be more potent and safe than digoxin. Its higher efficacy could be due to its structural specificity and might have been mediated through its better free radical scavenging action.     

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。     

异丙肾上腺素诱导慢性心力衰竭大鼠心肌醛固酮及其核受体的变化

目的 探讨异丙肾上腺素(isoproterenol,ISO)诱导的慢性心力衰竭SD大鼠心肌醛固酮及其核受体的变化.方法 将SD大鼠抽签随机分为心力衰竭组(9只)和对照组(10只),心力衰竭组皮下注射ISO,对照组皮下注射等量生理盐水,心功能采用超声心动图及血流动力学检查,放射免疫法测定血浆及心肌组织醛固酮水平,免疫印迹和免疫组化染色法检测盐皮质激素核受体蛋白表达的变化.结果 心力衰竭组与对照组比较心功能明显下降,左心室射血分数分别为(38.8±4.0)%与(79.4±4.6)%;左心室内压最大上升速率分别为(7164.4±502.6)mm Hg(1 mm Hg=0.133 kPa)/s与(10199.5±462.9)mm Hg/s(均P＜0.01).血浆及心肌组织醛固酮含量明显升高,分别为(0.63±0.06)μg/L与(0.30±0.07)μg/L、(0.41±0.05)μg/kg与(0.08±0.01)μg/kg(均P＜0.01),左心室心肌醛固酮核受体蛋白表达增高(P＜0.01).结论 ISO可诱导SD大鼠出现类似扩张型心肌病的慢性心力衰竭表现,在这种心力衰竭模型中其循环和左心室心肌醛固酮水平明显升高,心肌醛固酮核受体表达上调,可能在心力衰竭的发生、发展中起着重要作用.

Abstract：

Objective To investigate the changes of cardiac aldosterone and mineralocorticoid receptor (MR) in Sprague-dawley (SD) rats with chronic heart failure (CHF) induced by isoproterenol (ISO). Methods The SD rats were randomly divided into CHF group (n=9) and normal control(NC) group (n=10). The experimental CHF group was induced by subcutaneous injection of ISO, and the NC group received same dose injection of sodium chloride. The heart function was evaluated with both echocardiography and hemodynamics. The contents of aldosterone in both plasma and heart were assessed by radioimmunoassay. The expression of MR was measured by Western blot and immunohistochemistry staining. Results Compared with NC group, the heart function was decreased in CHF group, the left ventricular ejection fraction was (38.8%±4.0%) in CHF and(79. 4%±4.6%), in NC group. The maximal rate of increase of ventricular pressure (+dp/dtmax) was (7164.4±502.6) mm Hg(1 mm Hg=0.133 kPa)/s in CHF and (10199.5±462.9) mm Hg/s in NC group (both P＜0. 01 ). The contents of aldosterone both in plasma and heart were higher in CHF group than in NC group [(0.63±0.06)μg/L vs. (0.3±0.07) μg/L, (0.41±0.05) μg/kgvs. (0.08±0.01)μg/kg, both P＜0. 01]. The MR expression was increased in CHF group versus in NC group (P＜0.01). Conclusions The heart function is decreased in rats with CHF induced by ISO, which is similar to dilated cardiomyopathy. The higher levels of aldosterone both in circulation and in heart as and well as MR expression upregulation in heart may play important roles in the pathogenesis of CHF induced by ISO.     

Effect of zinc on acute and chronic isoproterenol induced heart injury

Hypertensive male rats were injected with single or multiple injections of isoproterenol. Some of the rats were administered zinc parenterally.A significant increase in serum zinc concentration occurred after administration of zinc but not in zinc content of the heart. Acute isoproterenol injection induced a 5-fold increase in calcium content of the heart. Zinc treatment significantly reduced calcium content and increased zinc content of the injured heart.When isoproterenol was injected in rats pretreated and simultaneously administered zinc for a period of 14 days, zinc significantly reduced calcium content, collagen content and size of the necrotic area in the heart. Histopathology of heart of rats treated with both zinc and isoproterenol showed only foci of necrosis replaced with less organized granulation tissue, while isoproterenol alone induced confluent circumferential subendocardial necrosis with mature granulation tissue. The weight of the heart (wet, dry, relative) was not affected by zinc treatment. The weight of the adrenal, significantly increased by isoproterenol, was significantly less in zinc-treated animals.It is concluded that parenteral administration of zinc partially protects the heart against isoproterenol induced myocardial necrosis. Although the mechanism of this effect is still not quite clear, we propose that zinc decreases the isoproterenol-induced influx of calcium into the myocardium, thus lowering the imbalance between heart work and O₂-supply to the cardiac muscle.     

Effect of chronic smoking on lipid peroxidation and antioxidant status in gastric carcinoma patients

Oxidative stress plays an important role in malignant transformation and is postulated to be associated with increased lipid peroxidation. We determined the effects of chronic cigarette smoking on lipid peroxidation and antioxidant status in 100 male patients with gastric cancer and an equal number of age-matched healthy control subjects. The mean (SD) level of thiobarbituric acid reactive substances (TBARS) was higher in plasma (healthy non-smokers 3.1 [0.2]; healthy smokers 4.6 [0.2]; gastric cancer non-smokers 6.5 [1.0]; gastric cancer smokers 8.9 [3.1]) and erythrocytes (3.3 [0.6]; 4.6 [0.1]; 8.3 [0.9]; 13.2 [5.1]) from gastric cancer patients when compared with control subjects. TBARS level was higher in smokers than non-smoking gastric cancer patients. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-treansferase, reduced glutathione, and vitamins A, E and C were decreased in gastric cancer patients who were smokers as compared to other groups (p<0.001). Thus, there occurs lipid peroxidation and possible breakdown of antioxidant status in cigarette smoking, which may increase the risk of gastric cancer.     

大鼠急性心肌损伤E选择素和细胞因子的变化

目的观察异丙肾上腺素导致大鼠急性心肌损伤早期E选择素和细胞因子TNF-α、IL-1βmRNA的变化,进一步探讨E选择素和细胞因子TNF-α、IL-1β在异丙肾上腺素导致大鼠急性心肌损伤发生发展中的作用。方法将大鼠随机分为对照组(35只)和实验组(35只),实验组给予异丙肾上腺素(isoproterenol,Iso),对照组给予生理盐水,分别在给药后4、8、16、24、48h各取7只大鼠心脏,光镜下观察心肌形态结构病理改变,应用逆转录-聚合酶链反应(RT-PCR)检测心肌组织E选择素、TNF-α和IL-1βmRNA的表达。结果实验组4hE选择素mRNA表达与对照组比较差异无统计学意义(P>0.05),实验组E选择素mRNA表达8h开始升高,24h达高峰,48h恢复正常;实验组TNF-αmRNA表达4h已经升高,16h达高峰,24h到48h逐渐下降;实验组IL-1βmRNA表达4h已经升高,8h达高峰,16h到48h逐渐下降。结论E选择素和细胞因子TNF-α、IL-1β在大鼠急性心肌损伤的发生中具有重要意义。     

异丙肾上腺素致大鼠心肌损伤肥大时骨架蛋白的变化及意义

目的复制异丙肾上腺素(isoproteronol,Iso)致大鼠心肌损伤及肥大模型,观察细胞骨架蛋白微管蛋白(tubulin)、结蛋白(desmin)变化特点,探讨心肌支持蛋白在心肌肥厚过程中的关系和变化规律,为抑制心室肥厚的发生和发展提供实验依据。方法①将雄性Wistar大白鼠随机分成对照组和损伤肥大组(Iso组)。Iso组皮下多点注射中等剂量Iso,建立大鼠损伤、代偿性肥厚模型。②光镜观察心肌组织的病理变化。③RT-PCR法检测tubulin、desminmRAN表达。④免疫组化法检测tubulin、desmin蛋白表达。结果光镜下Iso组心肌组织有明显的损伤肥大及纤维化,tubulinmRNA(0.9252±0.3765)和desminmRNA(1.2453±0.5326)表达与对照组(0.6846±0.2372)和(0.7142±0.1416)比较明显升高,差异有统计学意义(t=2.3258,P<0.05;t=4.0972,P<0.01)。Iso组tubulin(0.75±0.32)和desmin(0.85±0.29)蛋白表达与对照组(0.56±0.25)和(0.64±0.31)比较,差异也有统计学意义(t=2.5627,P<0.05;t=2.7544,P<0.01)。结论Iso致大鼠心肌损伤肥大时,tubulin、desmin无论在蛋白水平,还是在基因水平都增加,提示异丙基肾上腺素对大鼠心肌tubulin、desmin蛋白水平和基因水平的影响是平行、一致的。     

Lipid peroxidation in nicotinamide-deficient and nicotinamide-supplemented rats with streptozotocin-induced diabetes

Reactive oxygen species have been related to the pathogenesis of various diseases, including diabetes mellitus. Nicotinamide has been used for the prevention of the diabetogenic effects of streptozotocin (STZ) in animals. In the present study we assessed the effect of diets with deficient, normal or 17-fold supplemented nicotinamide concentrations on the rate of lipopoeroxidation in animals with STZ-induced diabetes. Male Wistar rats were divided into three groups kept on one of the diets for six weeks: DD, diabetic rats on a nicotinamide-deficient diet; DN, diabetic rats on a normal nicotinamide diet; and DS, diabetic rats on a nicotinamide-supplemented diet. During the fourth week of the experiment all animals were fasted for 24 hours and injected into the tail vein with a single STZ dose (40 mg/kg weight). Eight animals from each of the six groups were then sacrificed 24 hours, 1 week and 2 weeks after STZ injection. Mean pancreatic thiobarbituric acid reactive substances (TBARS) (nmol/mg tissue) were significantly lower in the DS group (p < 0.05) compared to the DN and DD groups at 24 hours and during the first week. Hepatic TBARS concentrations (nmol/mg protein) did not differ between groups. Mean hepatic reduced glutathione (GSH) levels were significantly higher (46.76 ± 12.33 nmol/mg protein) in the DS group compared to the DD (32.90 ± 6.70) and DN (24.55 ± 6.41) groups, but only after the 24-hour period. Hepatic vitamin E consumption (Μg/g tissue) was considerable in the groups not supplemented with nicotinamide, whereas vitamin E levels were unchanged in the supplemented group. In contrast, plasma vitamin E levels were decreased in the normal and supplemented groups after 1 and 2 weeks. A higher N-methylnicotinamide excretion (μg/ 24 hours) occurred in the supplemented group. We conclude that, after induction of diabetes with STZ, nicotinamide supplementation protected from the damage caused by the toxic action of STZ, promoting lower lipid peroxidation. Received: 27 September 1999 / Accepted in revised form: 3 March 2000     

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。     

急性心肌梗死患者冠状动脉循环血线粒体偶联因子-6含量变化及意义

目的:研究急性心肌梗死(AMI)患者血清线粒体偶联因子-6(CF6)含量在冠状动脉循环中的变化。方法:用放免方法分别测定AMI患者与对照组冠状静脉窦、冠状动脉与外周血清中CF6浓度。结果:AMI患者冠状静脉窦、冠状动脉、外周静脉血清中CF6浓度较对照组差异均有统计学意义(P<0.01),AMI患者冠状静脉窦血清CF6较冠状动脉血清CF6明显升高,差异有统计学意义(P<0.01)。结论:AMI患者外周静脉、冠状动脉和冠状静脉窦血清CF6浓度明显增高,以冠状静脉窦血清CF6升高最明显。     

Comparative effects of acute vs. chronic oral amiodarone treatment during acute myocardial infarction in rats.

AIMS: This study investigated whether chronic and acute amiodarone treatment has differential effects on ventricular arrhythmogenesis during acute myocardial infarction in rats. METHODS AND RESULTS: Forty-six rats were randomly allocated into vehicle, chronic oral amiodarone (30 mg/kg daily for 2 weeks), or acute amiodarone (a single dose, 100 mg/kg). Five additional rats were sham-operated. Myocardial infarction was generated by left coronary artery ligation 2 weeks after chronic treatment. Amiodarone was administered acutely 5 min post-ligation. The electrocardiogram was recorded for 24 h, using an implanted telemetry transmitter. Episodes of ventricular tachyarrhythmias and mortality rates were analysed. Serum catecholamines and infarct size were measured 24 h post-ligation. No differences were found in infarct size. Compared with controls (22.7 +/- 10.9), there was a similar reduction in the number of tachyarrhythmia episodes after either chronic (2.6 +/- 1.6, P = 0.0011) or acute (3.6 +/- 1.7, P = 0.031) amiodarone administration. Norepinephrine levels were lower only after chronic treatment. Mortality in both amiodarone treatment arms was exclusively due to bradyarrhythmia secondary to cardiac failure, whereas mortality in controls was mainly attributed to tachyarrhythmic death. CONCLUSIONS: A rapid antiarrhythmic effect was observed after acute amiodarone administration in the rat. Norepinephrine levels decreased after chronic treatment and may be associated with bradyarrhythmic mortality.     

异丙肾上腺素致心肌肥厚对兔心传导系统的影响

目的通过对心肌肥厚兔模型进行电生理研究,探讨心肌肥厚对心传导系统的影响。方法雄性新西兰大耳兔24只,随机分为心肌肥厚组和对照组,每组各12只。经耳缘静脉注射异丙肾上腺素制备心肌肥厚模型。造模2周后行超声检查评价造模结果。对所有动物行在体电生理检查,测量两组动物心房有效不应期(AERP)、房室结有效不应期(AVERP)、房室结反向传导有效不应期(VAERP)、窦房传导时间(SACT)、最大窦房恢复时间(SNRTMAX)、文氏周期长度(WCL),反文氏周期长度(RWCL)、房室2∶1传导频率等指标。结果心肌肥厚组AERP较对照组缩短(68.60±6.20 ms vs 77.30±12.30 ms,P<0.05),SACT、SNRTMAX、AVERP、WCL及房室2:1传导频率较对照组延长(分别为101.57±25.11 ms vs 78.33±25.17 ms,616.91±59.89 ms vs 540.64±83.18 ms,160.30±9.73 ms vs 133.80±3.89 ms,191.40±32.90 ms vs 151.10±24.30 ms,148.8±35.00 ms vs 137.30±23.40 ms,P均<0.05),而VAERP与RWCL较对照组则无明显变化(P>0.05)。结论心肌肥厚可导致心传导系统功能受损,为心肌肥厚时心律失常的发生提供条件。     

急性心肌梗死患者血清高敏肌钙蛋白T及线粒体偶联因子-6含量的变化

目的观察急性心肌梗死（AMI）患者血清高敏肌钙蛋白T（hs-TnT）及线粒体偶联因子-6（CF6）含量在冠状动脉循环中的变化。方法纳入2009年4月到2011年3月期间我院收诊的AMI患者60例,同期选取冠脉造影结果无狭窄或狭窄程度〈50%的患者30例作为对照组。取两组受试者冠状静脉窦、冠状动脉与外周血清,分别采用发光免疫法和放射免疫法测定hs-TnT及CF6浓度。结果 AMI患者冠状静脉窦、冠状动脉与外周静脉血清中hs-TnT、CF6浓度与对照组相比,差异均有统计学意义（P〈0.01）;AMI患者冠状静脉窦血清hs-TnT、CF6较冠状动脉血清hs-TnT、CF6均值升高,差异有统计学意义（P〈0.01）。结论 AMI可导致冠脉循环hs-TnT和CF6浓度升高,二者可在一定程度上预测心肌梗死面积。     

SHH信号通路激活对急性心肌梗死大鼠缺血心肌血管再生的作用

目的 探讨SHH(sonic hedgehog)信号通路激活对急性心肌梗死(AMI)大鼠缺血心肌血管再生作用及机制。方法 雄性成年SD大鼠80只,体质量（150~200）g采用结扎大鼠左前降支的方法制备AMI大鼠模型,随机分为单纯心肌梗死(AMI)组,外源性重组人SHH蛋白（rhSHH）处理组,SHH信号通路抑制剂Cyclopamine(CYC)处理组,连续处理7 d后,利用VIII因子免疫组织化学染色测定rhSHH对AMI大鼠缺血心肌微血管密度的影响;TTC染色观察各组心肌梗死面积;ELISA和RT-PCR方法测定AMI大鼠缺血心肌促血管再生相关的指标血管内皮生长因子(VEGF),碱性成纤维细胞生长因子(bFGF)及血管生成素(Ang)-1的血清和mRNA表达;Western blot检测各组SHH信号通路相关蛋白SHH,SMO,Gli-1的蛋白表达。结果 与AMI组相比,rhSHH处理后缺血心肌微血管密度显著增加（P<0.05）,心肌梗死面积减小（P<0.01）,血管生长因子VEGF,bFGF,Ang-1的血清水平和mRNA表达显著增加（P<0.01）,心肌梗死边缘区SHH信号通路下游靶分子(SHH,SMO,Gli-1)的蛋白表达显著增加（P<0.05）;这种影响可以被SHH信号通路抑制剂Cyclopamine所逆转（P<0.01）。结论 激活SHH通路可增加缺血心肌血管生长因子VEGF,bFGF,Ang-1的表达,促进急性心肌梗死大鼠的血管再生。     

Oxidative stress in portal hypertension-induced rats with particular emphasis on nitric oxide and trace metals

AIM: To investigate the oxidative-stress-related changes in rats with portal hypertension with particular emphasis on nitric oxide (NO) and trace metals. METHODS: Cirrhosis was induced by partial portal vein ligation (PVL) in Wistar rats. The lipid peroxidation marker (malondialdehyde, MDA), antioxidant defense enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and agents known to have antioxidant features including nitric oxide (NO), zinc (Zn), copper (Cu) were determined both in serum and in liver tissue at 4 wk after surgery in PVL and sham-operated rats. Portal pressure of all experimental animals was measured. MDA was detected by thiobarbituric acid reactivity assay. SOD activity was determined by inhibition of nitroblue tetrazolium reduction with xanthine/xanthine oxidase used as a superoxide generator. CAT activity was determined by the breakdown of hydrogen peroxide. GSH concentrations were measured by using metaphosphoric acid for protein precipitation and 5'-5'-dithio-bis-2-nitrobenzoic acid for color development. NO was detected by the Griess method after reduction of nitrate to nitrite with nitrate reductase, and the concentrations of Zn and Cu were measured by a Shimadzu 680 AA atomic absorption spectrometer. Histopathological confirmation was done under light microscope. Statistical analyses were done by Student's t-test, and significance of the difference was tested by the unpaired Mann-Whitney test. P<0.05 was considered statistically significant. RESULTS: Histopathological studies confirmed PVL-induced cirrhotic changes. There was a statistically significant difference in portal pressure between PVL and control groups (P<0.001). The results showed significant increases in the levels of MDA and NO in both tissue and serum (P<0.05 and P<0.001, respectively in tissue; P<0.001 for each in serum), and Zn only in tissue (P<0.001) in rats with PVL compared with sham-operated rats. Besides, PVL rats exhibited reduced plasma and tissue GSH, CAT, SOD (P<0.001 for each). Serum and tissue Cu concentration did not change. CONCLUSION: Our findings suggest that PVL in rats induces important biochemical and molecular changes related to oxidative stress in the liver.     

Influence of exercise training frequency on cardiac and hepatic oxidative stress in rats

The present study investigated the influence of different frequencies of moderate exercise (13 weeks of treadmill running at 60% of maximal oxygen consumption) on oxidative stress in the heart and liver in rats. Oxidative stress was evaluated by chemiluminescence and lipid peroxidation (LPO) through thiobarbituric acid reactive substances. Activities of superoxide dismutase (SOD), glutathione peroxidase (GHPx) and catalase (CAT) were also measured. The animals were divided into four groups: control (C), acute ([A], only one exercise session at the end of 13 weeks), low frequency ([LF], one session a week for 13 weeks) and high frequency ([HF], five sessions a week for 13 weeks). Chronic exercise promoted cardiac hypertrophy in the HF group. Myocardial LPO in groups A and LF was increased, whereas in the HF group, it was decreased when compared with group C. The HF group demonstrated decreased myocardial SOD and GHPx activities and increased CAT activity. All exercise groups exhibited an increase in LPO in the liver compared with group C. SOD activity in liver was lower in the HF group and higher in the LF group as compared with group C. GHPx activity was higher in group A in relation to group C. Hepatic CAT activity was higher in groups A, LF and HF. It is suggested that chronic exercise training at a submaximal level is better than infrequent exercise bursts to promote metabolic adaptations that minimize oxidative stress.     

慢性氟中毒大鼠肝脏损害机理及亚细胞部位研究

用３０ｍｇ／Ｌ，６０ｍｇ／Ｌ和１２０ｍｇ／Ｌ含氟水饲养大鼠１２周，复制慢性氟中毒动物模型，探讨肝脏损害机理和亚细胞部位、结果发现：肝损害指标肝甘油三酯（ＴＧ）含量和血清谷丙转氨酶（ＳＧＰ）活性显著升高；肝雨二醛（ＭＤＡ）含量显著升高，肝还原型谷胱甘肽（ＧＳＨ）含量显著降低；肝脂质过氧化指标变化与肝损害指标变化呈平行关系；肝线粒体和微粒体ＭＤＡ含量显著升高，其相应标志酶琥珀酸脱氢酶（ＳＤＨａｓｅ）和葡萄糖－６－磷酸酶（Ｇ－６－Ｐａｓｅ）活性显著降低，而且各亚细胞器ＭＤＡ含量升高分别与各自标志酶活性降低存在显著负相关关系。结果提示，慢性氟中毒引起肝脏损害机理之一是脂质过氧化；慢性氟中毒可致肝细胞线粒体和微粒体发生脂质过氧化损害作用。     

保心丸对大鼠心肌缺血再灌注心律失常的作用

目的观察保心丸对大鼠心肌缺血再灌注心律失常的作用，并探讨其作用机理。方法采用在体大鼠心肌缺血再灌注损伤模型，研究保心丸对再灌注心律失常，心肌超氧化物歧化酶（ＳＯＤ）活性和脂质过氧化产物丙二醛（ＭＤＡ）含量的影响。结果保心丸可明显缩短缺血再灌注心律失常的持续时间，降低室颤的发生率，提高心肌ＳＯＤ活性，降低ＭＤＡ含量。结论保心丸具有抗心肌缺血再灌注心律失常的作用，其机理与抑制脂质过氧化反应有关