The effect of crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart

Crataegus (Hawthorn) fruit extracts (CE) are widely used for the treatment of various cardiovascular diseases (arrhythmias, heart failure, myocardial weakness, etc). Despite the fact that many of these diseases are associated with disturbances of the mitochondria, no data have been found on the effect of CE on their function. The aim of this study was to perform an oxygraphic investigation of the effect of CE (in concentration range from 70 ng/mL to 13.9 µg/mL of Crataegus phenolic compounds (PC)) and its several pure flavonoids on isolated rat heart mitochondria respiring on pyruvate + malate, succinate and palmitoyl‐L‐carnitine + malate. CE at doses under 278 ng/mL of PC had no effect on mitochondrial functions. At concentrations from 278 ng/mL to 13.9 µg/mL of PC, CE stimulated State 2 respiration by 11%–34% with all used substrates, and decreased the mitochondrial membrane potential by 1.2–4.4 mV measured with a tetraphenylphosphonium‐selective electrode and H₂O₂ production measured fluorimetrically. Similar uncoupling effects on mitochondrial respiration were observed with several pure CE flavonoids. The highest CE concentration also slightly reduced the maximal ADP‐stimulated and uncoupled respiration, which might be due to inhibition of the mitochondrial respiratory chain between flavoprotein and cytochrome c. Whether or not the uncoupling and other effects of CE on mitochondria may be realized in vivo remains to be determined. Copyright © 2009 John Wiley & Sons, Ltd.     

Direct Effects of Vaccinium myrtillus L. Fruit Extracts on Rat Heart Mitochondrial Functions

In this study, the direct influence of bilberry (Vaccinium myrtillus) fruit extracts (aqueous and ethanolic) rich in anthocyanins on the oxidative phosphorylation of isolated rat heart mitochondria was investigated in vitro. Higher concentrations of bilberry extracts concentration‐dependently inhibited mitochondrial state 3 respiration (by 23%–61%) with pyruvate plus malate, mildly (by 1.2‐ to 1.3‐fold) uncoupled the oxidative phosphorylation, and increased (by 30%–87%) the state 4 respiration rate in the presence of exogenous cytochrome c. Succinate oxidation was less affected. Pure anthocyanins, the main components of used extracts, malvidin‐3‐glucoside, malvidin‐3‐galactoside, and cyanidin‐3‐galactoside, had no effect on oxidation of pyruvate plus malate. A statistically significant decrease in H₂O₂ production by mitochondria was found in the presence of bilberry fruit extracts. Our findings show that bilberry fruit anthocyanin‐rich extracts possess direct effects on rat heart mitochondrial function in vitro. These findings give the first insights into the mechanism(s) of their action on cellular energy metabolism. Copyright © 2012 John Wiley & Sons, Ltd.     

Uncoupling and antioxidant effects of ursolic acid in isolated rat heart mitochondria

Ursolic acid (1), a pentacyclic triterpene acid, is one of the major components of certain traditional medicinal plants and possesses a wide range of biological effects, such as anti-inflammatory, antioxidative, and cytotoxic activities. Furthermore, 1, when present at 1.6-5 ng/mL concentrations in commercial herbal preparations used for patients with cardiac disorders, may also exert pro-cardiac activities. There are several indirect suggestions that the cardioprotective mechanism of ursolic acid could involve the mitochondria; however the mechanism of action is still not known. Therefore, the effects of 0.4-200 ng/mL ursolic acid (1) on the functions of isolated rat heart mitochondria oxidizing either pyruvate and malate, succinate, or palmitoyl-l-carnitine plus malate were investigated. It was found that 1 induced a statistically significant uncoupling of oxidative phosphorylation. A statistically significant decrease in H?O? production in the mitochondria was observed after incubation with 5 ng/mL 1. This effect was comparable to the effectiveness of the classical uncoupler carbonyl cyanide 3-chlorophenylhydrazone. Since mild mitochondrial uncoupling has been proposed as one of the mechanisms of cardioprotection, the present results indicate that ursolic acid (1) has potential use as a cardioprotective compound.     

竹节参总皂苷预处理对冠脉结扎致大鼠急性心肌缺血损伤的影响

目的:研究竹节参总皂苷预处理对冠脉结扎致大鼠急性心肌缺血损伤的影响,并初步探讨其可能的机制。方法:实验大鼠随机分为假手术组、模型组和竹节参总皂苷组;治疗组大鼠给予竹节参总皂苷,预防性给药7 d后,行结扎大鼠冠状动脉术制作急性心肌缺血损伤模型,术后12 h进行大鼠心电图和血流动力学检测,然后取血进行血液乳酸脱氢酶(LDH)、肌酸激酶(CK)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量分析;取心脏,分别进行心肌组织2,3,5-氯化三苯基四氮唑染色和HE染色。结果:竹节参总皂苷能明显改善心功能,对抗冠脉结扎诱导的心电图T波降低,显著降低心肌梗死面积,减少心肌缺血性损伤;降低血清中CK、LDH活性和MDA含量,增加血清中SOD、CAT活性。结论:竹节参总皂苷对冠脉结扎致急性心肌缺血损伤具有较好的保护作用,抗氧化损伤可能是其作用机制之一。     

Cardioprotective effects of the combined use of puerarin and Danshensu on acute ischemic myocardial injury in rats

Ischemic heart diseases are the leading cause of death in both developed and developing countries over the past decades. The aim of this study was to investigate the cardioprotective effects of the complex preparation (called Shenge), made of puerarin and Danshensu, on acute ischemic myocardial injury in rats and its underlying mechanisms. The left anterior descending (LAD) coronary artery was occluded to induce myocardial ischemia in hearts of SD rats. Shenge was injected into the tail vein 15 min after occlusion at doses of 0, 30, 60 or 120 mg/kg. Then, the ST elevation was measured at 60, 120 and 240 min after Shenge administration. The infarct size, serum levels of creatine kinase isoenzyme-MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA), and the ST elevation were measured after the rats were killed. Shenge decreased the ST elevation induced by acute myocardial ischemia, reduced infarct size, serum levels of CK-MB, LDH and MDA and increased the serum activity of SOD in a dose-dependent manner. The combined use of puerarin and Danshensu at a ratio of 1:1 shows the most effective activity. In conclusion, Shenge exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, likely through its antioxidant and antilipid peroxidation properties, and thus may be used as an effective and promising medicine for both prophylaxis and treatment of ischemic heart disease.     

Antiinflammation Effects and Mechanisms Study of Geniposide on Rats with Collagen‐Induced Arthritis

Geniposide (GE), an iridoid glycoside compound purified from Gardenia jasminoides Ellis, has antiinflammatory and other pharmacological effects, but its mechanism of actions on rheumatoid arthritis (RA) have not been clarified. The purpose of this article was to investigate the pharmacological effects of GE on collagen‐induced arthritis (CIA) rats and its feasible mechanisms. Collagen‐induced arthritis was induced by injection of chicken type II collagen emulsion. The rats were orally administered with GE (33, 66, and 132 mg/kg) from days 14 to 30 after immunization. The histological examination showed that GE could attenuate histopathologic changes of mesenteric lymph node (MLN) in CIA rats. Geniposide inhibited the production of Interleukin 6 (IL‐6) and IL‐17, while promoting the production of IL‐4 and transforming growth factor‐beta 1 in MLN lymphocytes (MLNLs). Moreover, the proliferation capability of MLNLs was increased after the administration of GE. In addition, the treatment with GE in vivo decreased the expressions of P‐Raf, P‐MEK, and P‐Erk1/2 in MLNLs. These results may highlight the antiinflammatory effects and possible mechanisms of GE in MLNLs of RA. Copyright © 2017 John Wiley & Sons, Ltd.     

Mulberrofuran G Protects Ischemic Injury‐induced Cell Death via Inhibition of NOX4‐mediated ROS Generation and ER Stress

The aim of this study was to investigate the neuroprotective effect of mulberrofuran G (MG) in in vitro and in vivo models of cerebral ischemia. MG was isolated from the root bark of Morus bombycis. MG inhibited nicotinamide adenine dinucleotide phosphate oxidase (NOX) enzyme activity and oxygen–glucose deprivation/reoxygenation (OGD/R)‐induced NOX4 protein expression in SH‐SY5Y cells. MG inhibited the expression of activated caspase‐3 and caspase‐9 and cleaved poly adenine dinucleotide phosphate‐ribose polymerase in OGD/R‐induced SH‐SY5Y cells. In addition, MG protected OGD/R‐induced neuronal cell death and inhibited OGD/R‐induced reactive oxygen species generation in SH‐SY5Y cells. In in vivo model, MG‐treated groups (0.2, 1, and 5 mg/kg) reduced the infarct volume in middle cerebral artery occlusion/reperfusion‐induced ischemic rats. The MG‐treated groups also reduced NOX4 protein expression in middle cerebral artery occlusion/reperfusion‐induced ischemic rats. Furthermore, protein expression of 78‐kDa glucose‐regulated protein/binding immunoglobulin protein, phosphorylated IRE1α, X‐box‐binding protein 1, and cytosine enhancer binding protein homologous protein, mediators of endoplasmic reticulum stress, were inhibited in MG‐treated groups. Taken together, MG showed protective effect in in vitro and in vivo models of cerebral ischemia through inhibition of NOX4‐mediated reactive oxygen species generation and endoplasmic reticulum stress. This finding will give an insight that inhibition of NOX enzyme activity and NOX4 protein expression could be a new potential therapeutic strategy for cerebral ischemia. Copyright © 2016 John Wiley & Sons, Ltd.     

温阳益心中药对梗死大鼠心肌超微结构的影响

目的观察温阳益心中药对梗死大鼠心肌超微结构的影响,探讨其对心肌缺血-再灌注（IR）大鼠心肌的保护作用及其与心肌缺血预适应（IP）保护机制的关联性。方法选用雄性Wistar大鼠,随机分为4组,其中3组正常喂食,1组灌胃中药悬液,10d后建立大鼠心肌缺血模型。IR组：心肌缺血45min,再灌注48h。温阳益心中药预处理缺血-再灌注组（中药组）：每日灌胃温阳益心中药悬液0．36g／100g,连续10d;心肌缺血45min,再灌注48h。预适应处理缺血一再灌注组（IP组）：心肌缺血5min,再灌注5min,重复3次,然后心肌缺血45min,再灌注48h。采用电镜技术观察各组大鼠心室心肌超微结构改变。结果IR组肌膜破损,肌丝溶解断裂,排列松散,线粒体排列紊乱,有的线粒体呈空化或局部空化状,有的呈凝聚状,糖原减少。心肌损害较重,证实心肌缺血-再灌注后部分心肌坏死。中药组、IP组心肌细胞状态有所改善,肌膜完整,心肌细胞核呈椭圆形,核仁明显,线粒体较为明显,肌丝排列较为整齐,肌节明暗带清晰可见,线粒体较为整齐地排列在肌原纤维之间,但仍可见有些肌丝断裂及个别线粒体部分空化。结论心肌缺血预适应和温阳益心中药预处理可以通过减轻心肌超微结构损伤而保护缺血心肌,且二者对缺血再灌注大鼠心肌的超微结构损伤保护效应相近。     

Cardioprotective effect of sasanquasaponin preconditioning via bradykinin‐NO pathway in isolated rat heart

Sasanquasaponin (SQS) is an effective component of Camellia oleifera Abel. This study was designed to investigate the cardioprotective effect of SQS against ischemia‐reperfusion (I/R) injury and the possible mechanism in isolated rat hearts. These hearts were pretreated by SQS only or SQS and HOE140 in different groups, and then subjected to I/R injury. Hemodynamic parameters, oxidative injury, and NO level were measured. The results showed that SQS preconditioning could decrease the incidences of arrhythmias and improve the heart functions. In addition, SQS preconditioning could protect isolated I/R injured heart against lipid peroxidation, as evidenced by increases in SOD and GSH‐Px activity, and by decreases in contents of MDA, ROS generation. However, HOE140 treatment reversed all these indexes. NO production was significantly decreased after a treatment with HOE140. So we can propose that SQS preconditioning could induce the cardioprotective effects and the possible mechanism was that the activation of bradykinin‐NO system by SQS preconditioning had an inhibition effect on ROS generation in isolated heart. Copyright © 2009 John Wiley & Sons, Ltd.     

黄芪中不同提取成分对在体大鼠心肌缺血-再灌注损伤的心功能影响

目的 :观察黄芪中不同提取成分对心肌缺血 再灌注损伤大鼠心功能的影响。方法 :通过结扎大鼠左室冠状动脉前降支造成心肌缺血 再灌注损伤模型 ,观察静脉内注射黄芪中不同提取成分对心肌缺血 再灌注损伤过程中血流动力学和缺血心肌Na⁺ K⁺ ATP酶活性、cAMP和丙二醛含量的影响。结果 :黄芪甲甙、总皂甙和总黄酮能够减轻心肌缺血 再灌注引起的左心室内压、左心室内压最大上升与下降速率振幅的下降 ;并能使缺血心肌组织中Na⁺ ,K⁺ ATP酶活性降低。另外 ,黄芪总皂甙能够增加缺血心肌组织中cAMP含量 ;黄芪总黄酮能够降低缺血心肌组织中丙二醛的含量。结论 :黄芪中不同提取成分对大鼠心肌缺血 再灌注引起心功能损害具有保护作用 ,其机制可能涉及到能量代谢的改善或自由基生成的抑制和氧自由基的清除。     

Dietary Phenolic Acids of Macrotyloma uniflorum (Horse Gram) Protect the Rat Heart Against Isoproterenol‐Induced Myocardial Infarction

The present study investigates the cardioprotective activity of the Macrotyloma uniflorum seed extract (MUSE) and its phenolic acids (p‐coumaric acid and ferulic acid) in isoproterenol (ISO)‐induced myocardial infarction in rats. The previously mentioned phenolic acids were isolated and quantified from MUSE by HPLC. Pretreatment of gemfibrozil (reference standard), MUSE (250 and 500 mg/kg) and the phenolic acids for 30 days to rats treated with ISO (85 mg/kg) on the last 2 days resulted in a significant attenuation of the ISO‐elevated levels of serum marker enzymes (aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase MB), total cholesterol, triglycerides, uric acid, C‐reactive protein and malondialdehyde and a restoration of the levels of the ISO‐depleted marker enzymes, reduced glutathione and the antioxidant enzymes—superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in heart. Restoration of the ISO‐altered electrocardiogram pattern and haemodynamic parameters (left ventricular end diastolic pressure, heart rate, systolic, diastolic and mean arterial pressure) was also brought about by treatment with MUSE and the phenolic acids. It may be concluded that MUSE treatment to ISO‐challenged rats exhibits a significant cardioprotective effect probably because of the potent antioxidant activity of its phenolic acids that salvage the myocardium from the deleterious effects of ISO. Copyright © 2016 John Wiley & Sons, Ltd.     

Tribulus terrestris (Linn.) Attenuates Cellular Alterations Induced by Ischemia in H9c2 Cells Via Antioxidant Potential

Tribulus terrestris L. was evaluated for its cardioprotective property against myocardial ischemia in a cell line model. Initially, methanolic extract was prepared and subjected to sequential extraction with various solvents. The extract with high phenolic content (T. terrestris L. ethyl acetate extract–TTME) was further characterized for its chemical constituents and taken forward for evaluation against cardiac ischemia. HPLC analysis revealed the presence of phenolic compounds like caffeic acid (12.41 ± 0.22 mg g^?1), chlorogenic acid (0.52 ± 0.06 mg g^?1) and 4‐hydroxybenzoic acid (0.60 ± 0.08 mg g^?1). H9c2 cells were pretreated with TTME (10, 25, 50 and 100 µg/ml) for 24 h before the induction of ischemia. Then ischemia was induced by exposing cells to ischemia buffer, in a hypoxic chamber, maintained at 0.1% O₂, 95% N₂ and 5% CO₂, for 1 h. A significant (p ≤ 0.05) increase in reactive oxygen species generation (56%), superoxide production (18%), loss of plasma membrane integrity, dissipation of transmembrane potential, permeability transition pore opening and apoptosis had been observed during ischemia. However, pretreatment with TTME was found to significantly (p ≤ 0.05) attenuate the alterations caused by ischemia. The overall results of this study partially reveal the scientific basis of the use of T. terrestris L. in the traditional system of medicine for heart diseases. Copyright © 2015 John Wiley & Sons, Ltd.     

长期饮酒大鼠缺血脑组织中Fas—L抗原表达及细胞凋亡的动态研究

目的研究长期饮酒大鼠局灶性脑缺血后Fas-L抗原和细胞凋亡在各时间段的表达。方法7.2%酒精代水自由饮用12周的大鼠用线拴法制备局灶性脑缺血模型,在缺血后不同时间(1,3,6 h)分别以免疫组织化学方法和TUNEL法动态检测Fas-L抗原表达和细胞凋亡情况。结果长期饮酒组大鼠缺血1 h,Fas-L抗原和凋亡细胞呈阳性,3 h达高峰,6 h减少。结论长期饮酒大鼠在脑缺血后Fas-L的阳性表达和细胞凋亡比正常大鼠脑缺血明显,且促使凋亡细胞迅速坏死。     

Effect of Ginkgo biloba extract on the rat heart mitochondrial function

Ginkgo biloba L. (Ginkgoaceae) originated from China, first introduced to Europe in the 18th century, it is now distributed all over the world. The leaves of Ginkgo biloba include a rich complex of active compounds responsible for various pharmacological properties. Ginkgo biloba extract improves blood circulation, protects against oxidative cell damage, blocks platelet aggregation that could be important for prevention of cardiovascular diseases. Therefore the fluid extract from Ginkgo biloba leaves was prepared and tested for it is effect on rat mitochondrial function. Our data showed that 0.5 microl/ml of GE (containing 0.57 ng/ml of rutin, 0.23 ng/ml of quercitrin, 0.105 ng/ml of hyperosid and 0.02 ng/ml of quercetin) had no effect on the State 2 respiration rate of mitochondria with all used substrates: pyruvate+malate, succinate and palmitoyl-L-carnitine. Further increase in GE concentration (2 and 4 microl/ml), increased the State 2 respiration rate with all respiratory substrates in a dose-dependent manner (by 35-116%). The State 3 respiration rate was not affected by GE. In order to identify which compounds of GE could be responsible for the observed effects, we measured the effect of pure flavonoids: rutin, quercetin, hyperosid and quercitrin on mitochondrial respiration. All flavonoids (except of hyperosid) at maximal used concentration, comparable/identical to that in GE, stimulated the State 2 respiration rate only by 8-20%, i.e. less effectively as compared to GE. Therefore, for the explanation of the GE-induced uncoupling of oxidative phosphorylation, other biologically active compounds of GE have to be taken into account in future studies.     

Cardioprotective effects of saponins from Panax japonicus on acute myocardial ischemia against oxidative stress-triggered damage and cardiac cell death in rats

Aim

To study the cardioprotective effects of saponins from Panax japonicus (SPJ) on acute myocardial ischemia injury rats induced by ligating of the left anterior descending branch (LAD), on the basis of this investigation, the possible mechanism of SPJ was elucidated.

Materials and methods

SPJ was identified by high performance liquid chromatography-evaporative light scattering detection. Male Sprague-Dawley rats (200–220 g) were randomly divided into four groups: sham-operated, LAD, LAD + l-SPJ (SPJ, 50 mg/kg/day, orally) and LAD + h-SPJ (SPJ, 100 mg/kg/day, orally). Before operation, the foregoing groups were pretreated with homologous drug once a day for 7 days, respectively. After twelve hours in LAD, the cardioprotective effects of SPJ were evaluated by infarct size, biochemical values, hemodynamic, and histopathological observations and the antioxidative and antiapoptotic relative gene expressions.

Results

SPJ significantly improved heart function and decreased infarct size; remarkably decreased levels of serum lactate dehydrogenase, creatine kinase, xanthine oxide and malondialdehyde content, increased contents of serum total antioxidant capacity, superoxide dismutase (SOD), glutathione peroxidase, catalase; quantitative real-time PCR results showed that SPJ might markedly reverse the down-regulated mRNA expressions of the SOD1, SOD2 and SOD3, ameliorate the increased Bax and caspase-3 mRNA expressions and decreased Bcl-2 mRNA expression and ratios of Bcl-2 to Bax. Histopathological observations provided supportive evidence for biochemical analyses, and with the dose of SPJ increasing, the aforesaid improvement became more and more strong.

Conclusions

The studies demonstrated that in ischemic myocardium, oxidative stress caused the overgeneration and accumulation of reactive oxygen species (ROS), which was central of cardiac ischemic injury. SPJ exerted beneficially cardioprotective effects on myocardial ischemia injury rats, mainly scavenging oxidative stress-triggered overgeneration and accumulation of ROS, alleviating myocardial ischemia injury and cardiac cell death.     

Asiatic Acid Reduces Blood Pressure by Enhancing Nitric Oxide Bioavailability with Modulation of eNOS and p47phox Expression in l‐NAME‐induced Hypertensive Rats

We investigated the effect of asiatic acid (AA) on hemodynamic status, vascular function, oxidative stress markers, endothelial nitric oxide synthase (eNOS), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit expression in N_ω‐nitro‐l ‐arginine methyl ester hydrochloride (l ‐NAME)‐induced hypertensive rats. Male Sprague–Dawley rats treated with l ‐NAME (40 mg/kg/day) in drinking water for 5 weeks showed significant increases in mean arterial pressure, heart rate, hindlimb vascular resistance, vascular dysfunction, superoxide anion (O₂^??) production, and plasma malondialdehyde. Moreover, NO metabolite (NOx) levels were reduced, aortic eNOS expression was downregulated, and NADPH oxidase subunit p47^phox was upregulated in hypertensive rats (p < 0.05). Hypertensive rats that were administered AA (10 or 20 mg/kg/day) for the last 2 weeks of the study showed significant improvement in hemodynamic status and vascular function. The antihypertensive effects of AA were associated with elevated plasma NOx levels, together with upregulation of eNOS expression. Decreased vascular O₂^?? production, consistent with downregulation of p47^phox expression, was also observed after AA treatment. Our results are therefore consistent with a model whereby AA reduces blood pressure by enhancing NO bioavailability. Copyright © 2014 John Wiley & Sons, Ltd.     

Inhibitory Effect of Ethanol Extract of Magnolia officinalis on Memory Impairment and Amyloidogenesis in a Transgenic Mouse Model of Alzheimer's Disease via Regulating β‐Secretase Activity

Alzheimer's disease (AD) is the most common form of dementia and is characterized by deposition of amyloid beta (Aβ) in the brain. The components of the herb Magnolia officinalis are known to have antiinflammatory, antioxidative and neuroprotective activities. In this study we investigated the effects of ethanol extract of M. officinalis on memory dysfunction and amyloidogenesis in a transgenic mouse model of AD. Oral pretreatment of ethanol extract of M. officinalis (10 mg/kg in 0.05% ethanol) into drinking water for 3 months inhibited memory impairment and Aβ deposition in the brain of Tg2576 mice. Ethanol extract of M. officinalis also decreased activity of β‐secretase, cleaving Aβ from amyloid precursor protein (APP), and expression of β‐site APP cleaving enzyme 1 (BACE1), APP and its product, C99. Our results showed that ethanol extract of M. officinalis effectively prevented memory impairment via down‐regulating β‐secretase activity. Copyright © 2012 John Wiley & Sons, Ltd.     

Anthocyanidin attenuates myocardial ischemia induced injury via inhibition of ROS‐JNK‐Bcl‐2 pathway: New mechanism of anthocyanidin action

Despite treatment options available to date, myocardial ischemia (MI) remains the leading cause of death worldwide. Studies are focused on finding effective therapeutic strategies against MI injury. Growing interest has been developed in natural compounds possessing medicinal properties with scarcer side effects. Here, we have evaluated the cardioprotective potential of anthocyanidin against MI injury and explored its underlying protective mechanism. Left anterior descending coronary artery was ligated to induce MI in mice. Neonatal mice cardiomyocytes were treated with H₂O₂ to induce oxidative stress (a major contributor to MI injury) in vitro. Anthocyanidin pretreatment significantly reduced the infarct size, preserved the cell viability, and protected against ischemia‐induced cardiac injury in treatment groups compared with the H₂O₂‐treated group in vitro. Measurement of reactive oxygen species (ROS) validated the strong antioxidant potential of anthocyanidin, as significant reduction in oxidative stress was observed in anthocyanidin‐pretreated groups. Mechanistically, pretreatment with anthocyanidin significantly subdued the activation of JNK (to p‐JNK) and elevated Bcl‐2 levels. Both in vivo and in vitro findings suggest that anthocyanidin can induce a state of myocardial resistance against ischemic insult. We have provided the experimental evidence for inhibition of ROS/p‐JNK/Bcl‐2 pathway being the underlying mechanism of action of anthocyanidin. Our results support the use of anthocyanidin as therapeutic strategy against MI injury.     

益心酮片对大鼠心肌缺血的保护作用

目的 :造成不同实验性心肌缺血模型 ,观察益心酮抗心肌缺血的作用。方法 :采用结扎法和药物法(垂体后叶素、异丙肾上腺素 )造成实验性急性心肌缺血模型 ,观测心电图、血流动力学和形态学指标。结果 :本药以 100 ,200mg·kg^-1的剂量给大鼠灌服 ,对结轧冠脉左前降支 30min所致缺血再灌注模型 ,有恢复心率、血压、左室舒张末期压、左室内压及其最大上升、下降速率 (±dp/dt_max)和心电图ST段的作用 ;亦能显著缩小冠脉结扎大鼠的心肌梗死面积 ;对注射垂体后叶素 (iv)和异丙肾上腺素 (ip)所致急性心肌缺血模型 ,有逆转ST段偏移与T波降低的保护作用。结论 :益心酮对实验性心肌缺血具有保护作用和治疗作用。     

参麦注射液对异丙肾上腺素诱导大鼠心肌缺血的保护作用

[目的]研究参麦注射液对异丙肾上腺素诱导大鼠心肌缺血的保护作用。[方法]皮下多点注射异丙肾上腺素(ISO)85mg/kg,每日1次,连续2 d,制备大鼠心肌缺血模型。记录大鼠心电图(ECG)的变化,观察血流动力学、超声心动图及心肌组织病理学的改变,并测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)及丙二醛(MDA)的活性以及心脏指数的改变。[结果]参麦注射液能够降低由ISO所致的心肌缺血大鼠ST段的抬高,明显改善左室功能,降低心肌组织病变程度,并且显著降低CK、LDH、MDA水平及心脏指数,增加SOD水平,与模型组比较有统计学意义(P0.05或P0.01)。[结论]参麦注射液对ISO诱导的大鼠心肌缺血有一定的保护作用。