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。     

白藜芦醇甙对大鼠心脏缺血/再灌注损伤的保护作用

本文利用冠脉结扎/放松方法和Langendorff灌注技术,建立在体和离体大鼠心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤模型,探讨白藜芦醇甙(polydatin)对大鼠I/R心肌损伤的保护作用及其机制.观察白藜芦醇甙对缺血和再灌注心律失常、心肌梗死面积、心脏收缩功能、心肌超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量、NO含量以及一氧化氮合酶(nitric oxide synthase,NOS)活性的影响.结果显示:与对照组相比,白藜芦醇甙组大鼠缺血和再灌注心律失常明显降低(P<0.05,P<0.01);心肌梗死面积显著减少(P相似文献   

黄芪皂苷IV对心肌缺血／再灌注损伤的保护及抗凋亡作用的研究

目的：探讨黄芪皂苷Ⅳ对大鼠心肌缺血／再灌注损伤的保护作用及抗凋亡作用。方法：研究黄芪皂苷Ⅳ对大鼠收缩压和舒张压的作用;建立大鼠心肌缺血／再灌注模型,在缺血前给予黄芪皂苷Ⅳ处理,观察心律失常的改变,测定血液中乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）和丙二醛（MDA）的变化,检测计算凋亡心肌细胞百分比及对P-STAT1、P-STAT3蛋白表达的调控作用。结果：黄芪皂苷Ⅳ可降低大鼠收缩压和舒张压,心肌缺血／再灌注前,预先给予黄芪皂苷Ⅳ有抗心律失常作用,降低血液中LDH和MDA含量,提高SOD活性,降低凋亡心肌细胞百分比,显著增加P-STAT1蛋白表达而同时降低P-STAT3蛋白表达。结论：黄芪皂苷Ⅳ对心肌缺血／再灌注损伤具有一定的保护作用,减少心肌细胞凋亡,其机制可能与抑制P—STAT1,诱导P—STAT3表达有关。     

一氧化氮、内皮素-1对大鼠肢体缺血/再灌注后脑损伤的影响

目的: 研究一氧化氮(NO)和内皮素-1(ET-1)在大鼠肢体缺血/再灌注(LI/R)后脑损伤中的作用,探讨NO/ET-1平衡关系的变化对脑损伤的影响.方法: 在大鼠LI/R损伤模型上,应用NO合成前体物质L-精氨酸(L-Arg)、一氧化氮合酶(NOS)抑制剂氨基胍(AG)、ETA受体阻断剂BQl23进行干预,观察血浆 NO、ET-1、MDA、XOD、SOD、LDH及脑组织tNOS、iNOS、cNOS、NO、ET-1、MDA、XOD、MPO、 SOD的变化.结果: 与对照组比较,I/R组血浆MDA、XOD、LDH及脑组织MDA、XOD、MPO升高,SOD活性降低(P<0.01),脑组织tNOS和iNOS明显升高,而cNOS明显降低(P<0.01),I/R组血浆及脑组织NO、ET-1增加,NO/ET-1比值降低,脑损伤加重.应用L-Arg及BQ123后,血浆及脑组织NO/ET-1比值较I/R组升高,脑损伤减轻,应用AG后,NO/ET-1比值降低,脑损伤进一步加重.结论: 肢体缺血/再灌注后,一氧化氮与内皮素-l的比值降低时脑损伤加重.     

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。     

三种鼠尾草注射液对大鼠心肌缺血再灌注损伤的保护作用

本文研究了云南产鼠尾草属药物滇丹参、甘西鼠尾、褐毛甘西鼠尾对急性心肌缺血再灌注损伤的保护作用 ,并与丹参进行对比其疗效的相似性。结扎大鼠冠脉左前降支 ,30分钟后剪断结扎线造成心肌缺血再灌注模型 ,经股静脉给药。测定再灌注 6 0分钟后血清中CK、LDH、SOD、GSH -Px和MDA含量。结果滇丹参、甘西鼠尾、褐毛甘西鼠尾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 0 1,P <0 0 5 ) ,与丹参有相似的抗心肌缺血再灌注损伤作用。     

维生素E在青年和老年大鼠肾脏缺血/再灌注损伤中的作用

目的:探讨维生素E(VE)在青年和老年大鼠肾缺血/再灌注损伤(RI/RI)中的作用。方法:采用夹闭双侧肾动、静脉45min后恢复血流的方法制作RI/RI模型,测定血清中尿素氮(BUN)、肌酐(Scr)、丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)、诱生型一氧化氮合酶(iNOS)浓度,免疫组化检测肾皮质热休克蛋白70(HSP70)表达。流式细胞术检测肾皮质细胞凋亡率。结果:缺血/再灌注(I/R)后BUN、Scr含量明显升高,老年I/R组MDA含量高于青年I/R组,SOD含量低于青年IR组,HSP70、NO以及肾皮质细胞凋亡率高于control组;VE可显著降低RI/RI大鼠BUN、Scr、MDA、iNOS水平,升高NO和SOD水平,增加HSP70的表达,降低肾皮质细胞凋亡率。结论:VE可通过促进肾组织HSP70的表达,增加NO和SOD水平,提高大鼠体内清除自由基的能力,从而对青、老年大鼠肾缺血/再灌注损伤(RI/RI)起到一定的保护作用。     

Protective effects of diosgenin in the hyperlipidemic rat model and in human vascular endothelial cells against hydrogen peroxide-induced apoptosis

Hyperlipidemia is a major cause of atherosclerosis and atherosclerosis-associated conditions in cardiovascular diseases. Oxidative stress, as a main risk factor causes vascular endothelial cell apoptosis, which is implicated in the pathogenesis of cardiovascular disorders. Diosgenin, an aglycone of steroidal saponins, has been reported to exert anti-proliferative and proapoptotic actions on cancer cells widely. In this study, we propose that diosgenin can protect the hyperlipidemic rats and prevent endothelial apoptosis under oxidative stress. We investigated the hypolipidemic and antioxidative effects of diosgenin on rats fed with high cholesterol and high fat diet for 6 weeks. Serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), glutathione peroxidase (GSH-PX), nitric oxide synthase (NOS), hepatic malondialdehyde (MDA), lipoprotein lipase (LPL), hepaticlipase (HL) and superoxide dismutase (SOD) activities were evaluated. Then we explored the effects and mechanism of diosgenin against hydrogen peroxide-induced apoptosis of human vein endothelium cells (HUVECs). Intracellular reactive oxygen species (ROS), glutathione (GSH), nitric oxide (NO), DNA fragment formation and mitochondrial membrane potentials (ΔΨm) were determined. Diosgenin treatment increased LPL, HL, SOD, GSH-PX and NOS activities, thus attenuated oxygen free radicals, decreased MDA, TC, TG and LDL-C levels in hyperlipidemic rats. Diosgenin pretreatment significantly attenuated H₂O₂-induced apoptosis in HUVECs, intracellular ROS, GSH depletion, DNA fragment formation, and restored NO, ΔΨm. These results suggested that diosgenin is a very useful compound to control hyperlipidemia by both improving the lipid profile and modulating oxidative stress and prevent H₂O₂-induced apoptosis of HUVECs, in partly through regulating mitochondrial dysfunction pathway.     

Protective effects of adenosine in rabbit sinoatrial node ischemia–reperfusion model in vivo: control of arrhythmia by hyperpolarization-activated cyclic nucleotide-gated (HCN)4 channels

Disturbance of cardiac rhythm is one of the consequences of myocardial ischemia/reperfusion injury. Many researchers have prompted considerable interests in developing therapeutic approaches for its control. In present study, we want to determine whether that adenosine pre- and postconditioning have protective effects on sinoatrial node ischemia/reperfusion injury on morphology, arrhythmia score, serological markers (CK-MB and cTnT), SOD activities, MDA levels and expression of HCN4 channels in SA node cells. According to the arrhythmia score recorded, whether adenosine used in terms of ischemia or reperfusion, the total number of arrhythmia was significantly reduced, as well as the number of its episodes was also markedly decreased. We have also shown a clear correlation between HCN4 channels expression and the dysfunction of SA node cells. HCN4 immunoreactivity decreased after adenosine pre- and postconditioning, but changes were significantly smaller in the cells of the SA node compared with cells of I/R group. The content of cTnT, CK-MB and MDA in adenosine pre- and postconditioning group reduced significantly; but the level of SOD increased significantly. Histological examination and electron microscopy observations found in adenosine pre- and postconditioning group sinoatrial node injury also mitigated. These findings suggested that adenosine pre- or postconditioning were to reduce the incidence of ischemia/reperfusion arrhythmias, reduce myocardial ischemia reperfusion injury. The mechanism was to stabilize the SA node cells membrane and one possible mechanism involves modulation of HCN4 channels in pacemaker cells of the sinoatrial node.     

白鲜皮水提物对大鼠心肌缺血再灌注损伤的保护作用

目的研究白鲜皮水提物对大鼠心肌缺血再灌注损伤的保护作用。方法 Wistar大鼠随机分为假手术组,模型组,阳性药组(地奥心血康)及白鲜皮低、中、高剂量组(白鲜皮水提物0.128、0.64、1.28 g/kg),每组6只。结扎冠状动脉左前降支制备大鼠心肌缺血再灌注损伤模型,观察给药后大鼠心电图ST段的改变,测量心肌梗死面积,观察大鼠心肌组织病理形态,检测大鼠血清CK,SOD活性、MDA含量。结果白鲜皮中、高剂量组给药后能明显减少心肌梗死面积,明显降低缺血30 min和再灌注120 min时ST段的抬高,并能降低大鼠血清中MDA含量,升高SOD活性,减少因缺血导致的心肌组织病理损害。结论白鲜皮水提物对大鼠心肌缺血再灌注损伤具有保护作用,其作用机制可能与保护心肌细胞功能、提高心肌抗氧化能力、清除氧自由基有关。