紫铆花素通过调节AMPK/GSK-3β信号通路抑制心肌缺血再灌注损伤

目的:研究紫铆花素对心肌缺血再灌注损伤的保护作用及其机制。方法:体外建立H9c2心肌细胞缺血再灌注模型,分为正常组、模型组、紫铆花素低、中和高剂量组(10,20和40μM)。检测细胞存活率,LDH释放水平,试剂盒检测MDA、SOD、IL-1和IL-6水平,蛋白印迹法检测Bax,Bcl-2蛋白的表达以及AMPK和GSK-3β磷酸化水平。结果:与模型组比较,紫铆花素能够提高细胞存活率,减少LDH水平,降低MDA、IL-1和IL-6,增加SOD水平。减少Bax,Caspase-3蛋白的表达,增加Bcl-2蛋白的表达,提高Bcl-2/Bax的比值(P0.05)。同时,紫铆花素能够剂量依赖性的促进AMPK和GSK-3β磷酸化。进一步研究发现,紫铆花素的保护作用以及对GSK-3β的促磷酸化被AMPK抑制剂Compound C抵消。结论:紫铆花素能减轻心肌缺血再灌注损伤,抑制心肌细胞凋亡,其作用机制可能通过激活AMPK/GSK-3β信号通路,减轻氧化应激水平有关。     

激活κ-阿片受体抑制小鼠心肌缺血再灌注损伤的作用及机制

目的:探讨外源性κ-阿片受体激动剂U50,488H对小鼠缺血再灌注损伤心肌的保护作用及其机制。方法:选择成年雄性C57小鼠40只,将其随机分为4组:假手术组(Sham),缺血再灌注组(I/R),κ-阿片受体激动剂U50,488H+I/R组(U+I/R),κ-阿片受体阻断剂nor-BNI+U50,488H+I/R组(N+U+I/R)。建立小鼠急性心肌缺血再灌注在体模型,通过小动物超声仪检测小鼠心功能,采用氯化三苯基四氮唑-伊文思蓝双染检测心肌梗死面积,检测血清心肌损伤物LDH活性和cTnI含量,Western-Blot检测Ca MKII和磷酸化Ca MKII的表达。结果:与Sham组相比,I/R组小鼠心功能下降,心肌梗死面积增加,血清LDH和cTnI水平升高(P0.05),心肌组织内磷酸化Ca MKII的表达明显增加(P0.05);与I/R组相比,U+I/R组心功能改善,心肌梗死面积减小,血清LDH和cTnI水平降低(P0.05),心肌组织内CaMKII磷酸化被抑制(P0.05)。给予nor-BNI后,上述U50,488H的作用均被阻断。结论:κ-阿片受体激活可抑制CaMKII磷酸化并抑制心肌缺血再灌注损伤,改善心功能。     

缺血预处理对小鼠心肌缺血再灌注损伤的保护作用研究

通过建立C57/B6雄性小鼠心肌缺血再灌注(ischemia-reperfusion,I/R)模型,探讨缺血预处理对小鼠心肌缺血再灌注损伤的保护作用。首先,将36只6~8周C57/B6雄性小鼠随机分为3组(n=12):假手术组(Sham组)、缺血再灌注组(I/R组)及缺血预处理组(Ipost组)。然后,利用苏木素伊红(hematoxylin and eosin,HE)染色、脱氧三磷酸尿苷缺口末端标记(Td T-mediated d UTP-biotin nick end labeling,TUNEL)染色、免疫组化及蛋白质印迹方法,对比3组小鼠的心肌病理学改变、心肌细胞凋亡情况、梗死心肌边缘区微血管密度(microvessel density,MVD)的变化,以及肿瘤相关蛋白质PTEN(phosphatase and tensin homolog deleted from chromosome 10,即人第10号染色体缺失的磷酸酶及张力蛋白同源基因的编码产物)、自噬相关蛋白质LC3I/II和腺苷酸活化蛋白激酶(5-AMP activated protein kinase,AMPK)的表达水平。结果显示,I/R组心肌组织细胞水肿、炎症细胞浸润等组织病理学变化情况较Sham组明显,而Ipost组中的情况相比I/R组有明显改善;同时,Ipost组心肌凋亡率高于Sham组,但显著低于I/R组(P0.01);Ipost组梗死心肌边缘区域的微血管密度显著高于I/R组(P0.01)。此外,缺血预处理后,PTEN的表达水平降低,AMPK磷酸化水平以及LC3I/II蛋白的表达水平均增强。由此可见,缺血预处理可减轻I/R损伤,减少心肌梗死面积,减轻心肌水肿,对心肌细胞有明显的保护作用,其机制可能与梗死心肌中PTEN表达下调、AMPK磷酸化水平增强、心肌细胞自噬增强和凋亡减少有关。     

单磷酰脂A对大鼠心肌缺血/再灌注损伤的保护作用

目的:探讨丝裂素活化蛋白激酶P38MAPK是否参与单磷酰脂A预处理的延迟保护作用.方法:建立大鼠心肌缺血/再灌注损伤模型.应用单磷酰脂A及P38的特异性抑制剂SB203580预处理,检测预处理后不同时间点P38磷酸化水平,并观察各组单磷酸酰酯A预处理24 h后缺血/再灌注心肌的梗死范围LDH释放.结果:预处理后24 h其心梗范围缩小,血浆LDH活性升高程度减轻(分别P＜0.01,vs I/R).用P38的特异性抑制剂SB203580可消除预处理后的延迟保护作用.结论:①单磷酰脂A预处理对24 h后缺血/再灌注心肌有保护作用.②P38参与单磷酰脂A预处理后的延迟保护作用,P38短暂而快速的激活可能是药物延迟保护作用的重要机制之一.     

褐毛甘西鼠尾注射液对大鼠在体心肌缺血再灌注损伤的保护作用

本实验与丹参进行对比研究云南产鼠尾草属药物褐毛甘西鼠尾对急性心肌缺血再灌注损伤的保护作用。采用结扎大鼠冠脉左前降支方法造成心肌缺血再灌注模型,测定再灌注60 min后血清中CK、LDH、SOD、GSH-Px和MDA含量。实验结果显示:该药可以显著降低心肌缺血再灌注后血清CK、LDH和MDA含量,升高血清SOD和GSH-Px活力(P<0.01,P<0.05)。表明褐毛甘西鼠尾对在体缺血/再灌注心肌有保护作用。     

依达拉奉通过JNK对大鼠离体心肌缺血再灌注损伤的保护作用

目的:研究依达拉奉(Edaravone)对大鼠离体心肌缺血再灌注损伤的保护作用.方法:将54只SD大鼠随机分为3组,包括对照组(control group),缺血再灌注组(I/R group),依达拉奉组(Ed group).灌注液为K-H液,37℃下建立心肌缺血再灌注模型,预灌注15min,缺血30min,再灌注40 min,分别测量①复灌20和40min时心功能指标:心率(HR)、左室收缩压(LVDP)、左室舒张末压(LVEDP)、心室内压最大变化速率(±dp/dtmax),②复灌20和40 min时肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,③复灌40 min时超氧化物歧化酶(SOD)活性和和丙二醛(MDA)浓度,④复灌40min时心肌梗死面积,⑤复灌40min时心肌组织中JNK的磷酸化水平.结果:①依达拉奉组的±dp/dtmax明显回升(P<0.05),同时LVEDP、LVDP等指标也有明显改善(P<0.05);②再灌注40min时,与缺血再灌注组比,依达拉奉明显降低LDH和CK;③依达拉奉能显著降低MDA浓度,同时提高SOD水平(P<0.05);④依达拉奉组心肌梗死面积小于缺血再灌注组(P<0.05);⑤依达拉奉降低缺血心肌组织中磷酸化JNK的水平(P<0.05).结论:依达拉奉可以改善缺血心肌的血流动力学,增加心肌收缩力,减少心肌梗死面积;能发挥清除氧自由基,扭转氧化与抗氧化平衡系统失调的作用;其对离体心肌缺血再灌注的保护作用可能与JNK途径密切相关.     

缺血预处理对缺血/再灌注离体心脏的保护作用

目的：探讨连续多次短暂缺血预处理对缺血/再灌注损伤心肌的保护作用及机制。方法：采用大鼠离体心脏Lan-gendorff灌流模型,观察缺血预处理对心肌缺血/再灌注后不同时间点冠脉流出液中AST、CPK、UDH及冠脉流量,心肌组织中SOD、LPO以及再灌注性心律失常的影响。结果：缺血预处理可以减少缺血/再灌注损伤的心肌冠脉流出液中AST、CPK、LDH的含量,提高心肌SOD活性,降低LPO水平,并且抑制再灌注性心律失常的发生,提高再灌注期间的冠脉流量。结论：缺血预处理对心肌缺血/再灌注损伤具有一定保护作用。     

藏药莪达夏醇提物对大鼠心肌缺血-再灌注损伤的保护作用

本实验探讨藏药莪达夏对大鼠急性心肌缺血再灌注损伤的抗氧化保护作用。采用结扎大鼠冠脉左前降支方法造成心肌缺血再灌注模型,测定再灌注40 min后血清中乳酸脱氢酶(LDH)、肌酸激酶(CK)、超氧化物歧化酶(SOD)、谷肤甘肤过氧化物酶(GSH-Px)活性以及MDA含量。实验结果显示莪达夏可以显著降低心肌缺血再灌注后血清CK、LDH和MDA含量,升高血清SOD和GSH-Px活力(P0.01,P0.05)。表明藏药莪达夏对缺血-再灌注心肌损伤有抗氧化保护作用。     

缺血后处理、ATP后处理减轻兔缺血再灌注损伤:与腺苷受体激活有关

目的:近期实验研究显示,在再灌注的早期给予短暂、重复的缺血再灌(缺血后处理Postconditioning)能够减轻心肌再灌注损伤。本实验旨在探明三磷酸腺苷(ATP)用于缺血后处理是否产生上述保护效应,以及了解腺苷受体在此保护作用机制中的地位。方法:家兔开胸后左前降支均给予40min结扎和180min的再灌注,并随机分为5组:(1)对照组;(2)缺血后处理组;(3)ATP后处理组;(4)缺血后处理 SPT(硫苯茶碱)组;(5)SPT对照组。于实验终点测定心肌梗死面积(TTC染色),血浆CK-MB、SOD、MDA含量。结果:和时照组相比,缺血后处理组与ATP后处理组心梗面积减少(p<0．05),CK-MB也显著降低(p相似文献   

人参茎叶皂甙对高胆固醇饮食大鼠再灌注性心律失常和脂质过氧化的影响(英文)

研究人参茎叶皂甙(GSL)对高胆固醇饮食大鼠心肌再灌注性心律失常(RPA_r)和脂质过氧化的影响。方法:将胆固醇乳剂用灌胃法饲养大鼠14d,建立高脂血症模型,各组大鼠进行心肌缺血再灌注实验,观察高脂血症和GSL对大鼠心肌缺血再灌注2h后血丙二醇(MDA),超氧化物歧化酶(SOD)和一氧化氮(NO)水平的影响和对再灌注性心律失常发生率的影响。结果显示:(1)用胆固醇乳剂饲养大鼠14d,成功建立高脂血症模型。同时给予GSL14d有明显降脂作用。(2)高脂血症状态下,心肌缺血再灌注2h后,血MDA升高(p<0.01),SOD降低(p<0.01)和NO(p<0.05)降低,再灌注10min内RPAr的发生率增高。(3)GSL组再灌注后2h的血MDA降低,而SOD和NO水平显著升高;使RPAr发生率大为降低,无VF发生。实验显示高脂血症加重心肌缺血再灌注损伤和提高RPAr发生率及动物死亡率,GSL可减少高脂饮食大鼠脂质过氧化和诱导体内NO生成而减轻缺血再灌注心肌损伤,降低缺血再灌注性心律失常发生率。     

刺槐素对大鼠心肌缺血再灌注损伤的保护作用与机制研究

摘要 目的：探讨刺槐素对大鼠心肌缺血再灌注损伤(MIRI)的作用以及可能的作用机制。方法：对24只Sprague-Dawley (SD)大鼠进行随机分组,分为：假手术组、模型组、刺槐素给药组、刺槐素+AG490给药组,每组6只,通过结扎冠状动脉左前降支,缺血30 min,再灌注120 min复制心肌缺血再灌注损伤模型。利用氯化三苯基四氮唑测定心肌梗死面积,紫外分光光度计和酶联免疫法检测血清中肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）的活性,蛋白印迹法分别检测心肌组织中Bcl-2、Bax、Stat3和p-Stat3蛋白相对表达水平。结果：与假手术组比较,模型组大鼠血清中CK-MB、LDH活性明显升高（P＜0.01）,心肌梗死面积百分比显著增加（P＜0.01）,p-Stat3/Stat3比率、Bcl-2/Bax比率显著下降（P＜0.01）;与模型组相比,刺槐素给药组中CK-MB、LDH的活性,以及心肌梗死面积百分比显著降低（P＜0.01）,Bcl-2/Bax比率和p-Stat3/Stat3比率显著提高（P＜0.05）。然而在刺槐素+AG490药物组中刺槐素对于受损心肌的保护作用被AG490消除。结论：刺槐素可减轻MIRI大鼠心肌损伤,发挥心肌保护作用,其机制可能与活化Jak2/Stat3信号通路进而抑制心肌细胞凋亡有关。     

楤木皂苷对大鼠心肌缺血/再灌注损伤的保护作用

目的:观察楤木皂苷(total saponins extracted from Aralia taibaiensis,s AT)对大鼠心肌缺血/再灌注(myocardia1 ischemia/reperfusion,MI/R)损伤的影响。方法:可逆性冠脉左前降支结扎缺血30 min再灌注3 h复制MI/R模型,将SD大鼠随机分为假手术组、模型组、s AT低、中、高剂量组,每组10只。采用伊文思蓝(EB)、2,3,5-氯化三苯基四氮唑蓝(TTC)双染法测定心肌梗死面积,苏木精-伊红(HE)染色法观察心肌病理学形态变化,并检测血清中乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)、超氧化物歧化酶(SOD)、丙二醛(MDA)、过氧化氢酶(CAT)及谷胱甘肽过氧化物酶(GSH-Px)水平。结果:与模型组比较,s AT中、高剂量组可明显缩小心肌梗死面积(P0.05),并显著降低血清中LDH、CK-MB及MDA的含量,同时使得血清中SOD、CAT和GSH-Px的活性增加。且所有给药组心肌组织的病理损伤也小于模型组。结论:s AT对大鼠MI/R损伤具有保护作用,其机制可能与抗氧化作用相关。     

Enhancing AMPK activation during ischemia protects the diabetic heart against reperfusion injury

AMPK activation during ischemia helps the myocardium to cope with the deficit of energy production. As AMPK activity is considered to be impaired in diabetes, we hypothesized that enhancing AMPK activation during ischemia above physiological levels would protect the ischemic diabetic heart through AMPK activation and subsequent inhibition of mitochondrial permeability transition pore (mPTP) opening. Isolated perfused hearts from normoglycemic Wistar or diabetic Goto-Kakizaki (GK) rats (n ≥ 6/group) were subjected to 35 min of ischemia in the presence of 10, 20, and 40 μM of A-769662, a known activator of AMPK, followed by 120 min of reperfusion with normal buffer. Myocardial infarction and AMPK phosphorylation were assessed. The effect of A-769662 on mPTP opening in adult cardiomyocytes isolated from both strains was also determined. A-769662 at 20 μM reduced infarct size in both Wistar (30.5 ± 2.7 vs. 51.8 ± 3.9% vehicle; P < 0.001) and GK hearts (22.7 ± 3.0 vs. 48.5 ± 4.7% vehicle; P < 0.001). This protection was accompanied by a significant increase in AMPK and GSK-3β phosphorylation. In addition, A-769662 significantly inhibited mPTP opening in both Wistar and GK cardiomyocytes subjected to oxidative stress. We demonstrate that AMPK activation during ischemia via A-769662 reduces myocardial infarct size in both the nondiabetic and diabetic rat heart. Furthermore, this cardioprotective effect appears to be mediated through inhibition of mPTP opening. Our findings suggest that improving AMPK activation during ischemia can be another mechanism for protecting the ischemic heart.     

Post-infarct treatment with [Pyr1]-apelin-13 reduces myocardial damage through reduction of oxidative injury and nitric oxide enhancement in the rat model of myocardial infarction

Apelin is a newly discovered peptide that has been recently shown to have cardioprotective effects in the animal model of myocardial infarction (MI) and ischemia/reperfusion (I/R) injuries. The aim of the present study was to investigate the long term cardioprotective effect of [Pyr1]-apelin-13 in the rat model of MI. Male Wistar rats (n = 22) were randomly divided into three groups: (1) sham operated group (2) control MI group and (3) MI treated with apelin (MI-AP group). MI animals were subjected to 30 min of left anterior descending coronary artery (LAD) ligation and 14 days of reperfusion. 24 h after LAD ligation, apelin (10 nmol/kg/day) was administered i.p. for 5 days. Blood sampling was performed at days 1, 3, 5 and 7 after MI for determination of serum changes of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), malondialdehyde (MDA) and nitric oxide (NO). Myocardial infarct size (IS) and hemodynamic function were also measured at the end of the study at day 14. We found out that post infarct treatment with apelin decreases infarct size, serum levels of LDH, CK-MB and MDA and increases heart rate and serum level of NO in the consecutive days, but there were no significant differences in blood pressure in the MI-AP group in comparison with MI. In conclusion, apelin has long term cardioprotective effects against myocardial infarction through attenuation of cardiac tissue injury and lipid peroxidation and enhancement of NO production.     

Protective effect of Salvia miltiorrhiza aqueous extract on myocardium oxidative injury in ischemic–reperfusion rats

Salvia miltiorrhiza has strong antioxidative activity. They may have a strong potential as cardioprotective agents in ischemic–reperfusion injury. Experiments were carried out in Sprague–Dawley rats with myocardium ischemia reperfusion (IR). Myocardial injuries during IR were determined by changes in electrocardiogram analysis of arrhythmias, antioxidant enzyme activities, AST, CK-MB, lactate dehydrogenase (LDH) levels, and myocyte apoptosis. Results showed that S. miltiorrhiza aqueous extract (SAME) pre-treatment significantly decreased the ST-segment (ΣST₁₂₀) and myocardium MDA, AST, CK-MB, lactate dehydrogenase (LDH) levels, increased myocardium antioxidant enzyme activities, and inhibit myocardium cell apoptosis. Furthermore, the SAME pre-treatment significantly upregulated p-JAK2 and p-STAT3 protein expression, decreased myocardium TNF-α and IL-6 concentrations in IR rats. The levels of TNF-α and IL-6 were positively correlated with the changes in myocardium p-JAK2 and p-STAT3 protein expression levels in IR rats. It can be concluded that the SAME pre-treatment has anti-ischemic and anti-apoptosis activity in heart IR rats. SAME pre-treatment protects heart against IR injury, at least in part, through its stimulating effects on injury-induced deactivation of JAK2/STAT3 signaling pathway.     

毛蕊异黄酮通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤的研究

目的:探讨毛蕊异黄酮抗脑缺血再灌注损伤的作用是否与抑制calpain-1的表达有关。方法:将SD大鼠随机分为假手术组、模型组以及药物组,采用线栓法建立大鼠大脑中动脉阻断(MCAO)模型,于缺血再灌注前30 min腹腔注射给予20 mg/kg毛蕊异黄酮或等体积的溶剂。再灌注24 h后,行神经功能学评分、脑梗死面积以及神经元凋亡检测;再灌注12 h、24 h时,采用免疫组化和蛋白印迹技术检测大鼠脑皮层calpain-1的表达。结果:与假手术组大鼠比较,MCAO模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率及calpain-1的表达均明显升高(P0.05),而毛蕊异黄酮能够降低模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率以及calpain-1的表达(P0.05)。结论:毛蕊异黄酮可能通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤作用。     

Protective effect of ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats

The objective of the current study is to investigate whether ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with ginsenoside Rb1 in the diabetic myocardium.     

Hypercholesterolemia Abrogates the Cardioprotection of Ischemic Postconditioning in Isolated Rat Heart: Roles of Glycogen Synthase Kinase-3β and the Mitochondrial Permeability Transition Pore

Ischemic postconditioning (IPO) reduces lethal reperfusion injury under normal conditions, but its effectiveness in hypercholesterolemia (HC) is disputed. We measured the cardioprotection of IPO in hypercholesterolemic rats and determined the roles of glycogen synthase kinase-3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP). Isolated rat hearts underwent 30-min global ischemia and 120-min reperfusion. Postconditioning protocol induced six cycles of 10s ischemia and 10s reperfusion at the onset of the reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride staining and cardiomyocyte apoptosis was assessed by TUNEL staining. GSK-3β phosphorylation was measured by immunoblotting. The opening of mPTP was measured by NAD⁺ content in myocardium. In normocholesterolemia (NC) groups, infarct size and cardiomyocyte apoptosis were significantly reduced after IPO. These reductions were completely abolished by HC, as evidenced by a similar infarct size and cardiomyocyte apoptosis observed between the IPO-HC and IR (ischemia–reperfusion)-HC groups. GSK-3β phosphorylation was significantly higher in the IPO-NC than the IPO-HC group. In addition, NAD⁺ content in myocardium, a marker of mPTP opening, was higher in the IPO-NC group than the IPO-HC group. In conclusion, cardioprotection of IPO is blocked by hypercholesterolemia. This might be due to the impairment of phosphorylation of GSK-3β and attenuation of mPTP opening.     

小鼠脑缺血再灌注模型稳定性研究

目的:探讨影响小鼠脑缺血再灌注模型成功率,梗死体积以及行为学评分稳定性的因素。方法:采用昆明小鼠75只,体重为20-23 g,随机分为5组,比较在不同长度的线栓以及不同进栓深度的条件下对小鼠脑缺血再灌注模型成功率,梗死体积以及行为学评分的稳定性的影响。同时术中行脑血流监测,比较各组小鼠大脑中动脉脑血流下降的差异。结果:规格1组,模型成功率为40%,梗死体积为(16.7±9.3)%,神经功能缺损评分(NSS):7.2±2.4,大脑中动脉(MCA)血流下降百分比:(86.9±4.2)%;规格2组,模型成功率为46.7%,梗死体积百分比为(19.2±11.6)%,NSS:8.8±2.5,MCA血流下降百分比:(87.4±3.8)%;规格3组,模型成功率为33.3%,梗死体积百分比为(16.6±9.6)%,NSS:8.2±2.6,MCA血流下降百分比:(88.3±3.4)%;规格4组,模型成功率为86.7%,梗死体积百分比为(23.4±2.2)%,NSS:13.9±1.3,MCA血流下降百分比:(87.5±3.5)%。结论:1.小鼠脑缺血再灌注模型稳定性关键因素在于线栓能对后交通动脉(PComA)和大脑前动脉(ACA)起始段形成有效栓塞。2.小鼠大脑中动脉血流监测并不能作为评价小鼠脑缺血再管注模型成功与否的主要依据。     

Cardioprotective effects of resveratrol following myocardial ischemia and reperfusion

Resveratrol (RSV), a plant origin polyphenol, has shown beneficial cardiovascular effects. In this study, isolated hearts from male Wistar rats were studied using the Langendorff technique. Following 30 min stabilization, the hearts underwent 30 min global ischemia and 120 min reperfusion. The perfusion solution in the test group contained RSV (10 μM). Hemodynamics of the hearts, the markers of myocardial damage including creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and troponin I were studied during the study. Furthermore, the infarct size and the markers of oxidative stress including catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) were assayed in the homogenates of the hearts. The release of nitrite from the hearts and the occurrence of ventricular arrhythmias were also monitored throughout the experiment. Resveratrol caused a significant improvement in the restoration of the mechanical performance of the hearts following myocardial ischemia and reperfusion (MIR). Besides, the infarct size, CK-MB, LDH, and troponin I declined in the test group. Besides, the cardiac release of nitrite increased, and the redox status of the heart was improved as indicated by the levels of CAT, SOD, GPX, and MDA. Finally, the treatment caused significant decreases in the occurrences of single and salvo arrhythmias, ventricular tachycardia, and ventricular fibrillation. The current study suggests strong cardioprotective and antiarrhythmic effects for RSV following MIR.