人参皂甙Rg1可促进大鼠心肌梗死后心肌再生

目的观察人参皂甙Rg1促进大鼠心肌梗死后缺血心肌的再生。方法结扎Wistar大鼠左冠状动脉制作急性心肌梗死（acute myocardial infarction,AMI）模型,随机分为治疗组和对照组,治疗组大鼠采用人参皂甙Rg1治疗。于建模后24h、2周和4周时杀死大鼠,取出心脏,HE染色观察细胞形态特征和心肌基本结构,并测量梗死面积,计算心室肌质量/体质量的比值、心肌梗死总面积/左心室肌总面积的百分比;免疫组织化学方法观察心肌组织CD34阳性细胞的表达;并比较治疗前后外周血中CD34阳性细胞数量的变化。结果应用人参皂甙Rg1治疗后,外周血中CD34细胞数量变化:治疗组,制模前:（0.043±0.023）%,24h:（0.202±0.081）%,2周:（0.937±0.142）%,4周:（0.834±0.110）%;对照组,制模前:（0.046±0.022）%,24h:（0.056±0.037）%,2周:（0.069±0.045）%,4周:（0.064±0.042）%;治疗组制模后24h、2周和4周的CD34阳性细胞百分率均比制模前和对照组大鼠的百分率明显升高（P<0.05）;治疗组大鼠在第2、4周时,心室肌质量/体质量均比对照组明显低（P<0.05）;治疗组大鼠心梗区可见大量CD34阳性细胞浸润,其梗死面积明显减小;治疗组大鼠心肌梗死程度较对照组减轻,其缺血心肌的基本结构得到保护。结论应用人参皂甙Rg1治疗AMI大鼠,能显著提高外周血的干细胞数量,并促进干细胞归巢梗死心肌、分化为心肌细胞样细胞,促进心肌再生缩小梗死面积,明显减轻心室重构,保护缺血心肌的基本结构。     

人参皂甙Rg1扩张兔基底动脉作用及其机制

目的 :观察人参皂甙 Rg1（G- Rg1）对基底动脉条的扩张作用 ,并探讨其作用机制。方法 :采用离体血管条灌流实验法 ,观察 G- Rg1对去甲肾上腺素 （NA ）、Ca Cl2 、KCl反应的影响 ,以及去除内皮细胞后 ,G- Rg1扩血管作用的变化。结果 :0 .1mm ol· L- 1及 0 .0 1mmol· L- 1 G- Rg1分别使 NA和 Ca Cl2 量效曲线明显右移 ,最大反应压低 ,非竞争性拮抗参数 p D2 ′分别为 3.6 4和 4.6 6。 G- Rg1对 NA依内 Ca2 +性收缩和依外 Ca2 +性收缩均具有显著的抑制作用。去除内皮可明显减弱 G- Rg1扩张 KCl诱导的收缩血管作用。结论 :G- Rg1既可通过抑制内 Ca2 +释放 ,也可抑制Ca2 +通过电压依赖性 Ca2 +通道的内流 ,舒张脑基底动脉 ,其舒张作用有内皮依赖性。     

人参皂甙Rg1对学习和记忆的改善作用与抗衰老机制的研究进展

人参皂甙是人参的主要活性成分，主要抗衰老有效成份人参皂甙Rg1是近年来研究的热点，我们就这方面的研究近况作一综述。     

人参皂苷Rb1对急性心肌梗死大鼠心室重构的影响

目的通过大鼠急性心肌梗死心室重构模型观察人参皂苷Rb1对心室重构的影响.方法结扎雄性SD大鼠左冠状动脉前降支制备急性心肌梗死(AMI)模型,随机分为AMI对照组(n=7)和人参皂苷Rb1治疗组(n=8,简称Rb1治疗组),另设假手术组(n=8).Rb1治疗组经腹腔注射人参皂苷Rb1(4mg·kg-1·d-1),假手术组及AMI对照组给予同量的0.9%氯化钠溶液,4周后检测大鼠血流动力学及形态学参数,免疫组化法检测左室非梗死区Ⅰ型胶原表达.结果与假手术组比较,AMI对照组左室重量指数、左室截面直径、Ⅰ型胶原含量及左室舒张末压(LVEDP)均明显增高,差异有非常显著性意义(P＜0.01),而左室收缩压(LVSP)及左室内压最大上升和下降速率均明显降低,差异有非常显著性意义(P＜0.01);与AMI对照组比较,Rb1治疗组左室重量指数、左室截面直径、Ⅰ型胶原含量及LVEDP、左室梗死面积均明显降低,差异有显著性意义(P＜0.01 或＜0.05),而LVSP及左室最大上升和下降速度均明显增高,差异有显著性意义(P＜0.05).三组间心率差异无显著性意义.结论人参皂苷Rb1能有效抑制急性心肌梗死大鼠的心室重构,保护心功能.     

人参皂甙Rg3对喉癌细胞黏附能力的影响

目的 观察人参皂甙Rg3对喉癌细胞系(Hep-2)铺展及黏附能力的影响.方法 人参皂甙Rg3作用于Hep-2细胞3 d后,观察其形态学变化;相差显微镜下观察其铺展情况;利用CCK8法检测其黏附能力的变化.结果 Hep-2在人参皂甙Rg3作用后,生长状态差;用药组较对照组铺展及黏附能力明显下降,均具有统计学意义(P<0.05).结论 人参皂甙Rg3能抑制Hep-2的铺展及黏附能力.     

人参皂甙—Rg3、—Rb3抗病毒作用的研究

目的 观察人参皂甙－Rg3,-Rb3抗病毒的活性。方法在FL细胞中扩增病毒,进行TCID50滴定,采用细胞病变抑制效应（CPE）的测定法观察药物的抗病毒作用。结果 0．125－4．0μg/ml浓度的人参皂甙－Rg3因浓度不同可以以不同方式抑制SV－1和PolioV致CPE发生;156．2－250μg/ml浓度的人参皂甙－Rb3因浓度不同可以不同方式抑制HSV－1和VSV致CPE发生。结论 人参皂甙－Rg3具有抗HSV－1和PoliⅤ活性,人参皂甙－Rb3具有抗HSV－1和VSV活性。     

人参皂甙Rg3对喉癌细胞迁移能力的影响

目的探讨人参皂甙Rg3对喉癌细胞株Hep2迁移能力的影响。方法人参皂甙Rg3作用于Hep2细胞后,利用划痕实验比较各组间细胞迁移能力的区别;同时检测基质金属蛋白酶(MMP2)的表达情况。结果用药组较对照组迁移能力下降,且RT-PCR检测结果显示用药组MMP2 mRNA的表达下调。结论人参皂甙Rg3能抑制Hep2的迁移能力,对肿瘤的浸润、转移有一定的抑制作用。     

人参皂甙Rg1对老龄脑缺血再灌注损伤大鼠脑功能的保护及谷氨酸、天冬氨酸含量的影响

目的探讨人参皂甙Rg1(GS Rg1)对老龄局灶性脑缺血再灌注损伤(IRI)大鼠脑功能的保护及脑组织谷氨酸(Glu)、天冬氨酸(Asp)含量的影响。方法将大鼠随机分为假手术组、模型组、血栓通注射液组及GS Rg1组(10、20、40 mg/kg),线栓法闭塞大鼠大脑中动脉2 h后再灌注建立局灶性脑缺血再灌注(IR)模型,在动物麻醉清醒后参考Longa 5分制法进行行为学评分,处死后取脑组织匀浆测定Glu、Asp的含量。结果与模型组比较,GS Rg1中剂量及大剂量组均降低神经行为学评分(P<0.05),降低脑梗死面积(P<0.05),降低脑组织中Glu及Asp含量(P<0.05,P<0.01)。结论 GS Rg1对IR老龄大鼠脑损伤存在保护作用,其机制可能是通过降低Glu及Asp水平实现。     

人参皂苷Rg1预处理对脂多糖诱导大鼠心肌细胞损伤的影响

目的探讨不同剂量人参皂苷Rg1预处理对培养乳鼠心肌细胞脂多糖（LPS）损伤的影响。方法取SD新生大鼠60只,分离心肌细胞培养,培养第4天随机分为4组（每次取12只,每组重复5次）：对照组、LPS组、低剂量人参皂苷Rg1（Rg110μmo1／L）＋LPS组、高剂量人参皂苷Rg1（Rg140μmo1／L）＋LPS组,分别观察各组心肌细胞搏动频率、细胞存活率和培养液中乳酸脱氢酶（LDH）活性、TNFα水平。结果①细胞搏动频率、细胞存活率：LPS组较对照组明显降低（P〈0．01）,人参皂苷Rg1＋LPS组较LPS组显著增高（P〈0．01）,高剂量人参皂苷Rg1组比低剂量组增高（P〈0．01）。②LDH活性：LPS组较对照组明显升高（P〈0．01）,人参皂苷Rg1＋LPS组与LPS组相比LDH明显降低（P〈0．01）,高剂量人参皂苷Rg1组较低剂量组低（P〈0．01）。③TNFα水平：与对照组相比,LPS组细胞悬液中TNFα增加（P〈0．01）,人参皂苷Rg1＋LPS组较LPS组明显减低（P〈0．01）;人参皂苷Rg1高剂量组较低剂量组低（P〈0．01）。结论人参皂苷Rg1对心肌细胞LPS损伤具有保护作用。     

人参皂苷Rg1对衰老大鼠胸腺结构与功能的影响

目的探讨人参皂苷Rg1对衰老大鼠胸腺结构与功能的影响及机制。方法 SD大鼠随机分为4组,每组10只。衰老模型组,皮下注射D-半乳糖120 mg/kg,1次/d,42 d;Rg1衰老模型组,注射D-半乳糖剂量与时间同衰老模型组,第15天起腹腔注射Rg1 20 mg/kg,1次/d,28 d正常对照组,皮下注射生理盐水1次/d,42 d;Rg1正常对照组,注射生理盐水1次/d,14 d,第15天起腹腔注射Rg1(同Rg1衰老模型组)。模型复制或药物注射完成后第2天,取胸腺测定胸腺指数,石蜡切片观察胸腺形态学;衰老相关β-半乳糖苷酶(SA-β-Gal)染色检测胸腺细胞衰老,CCK-8检测胸腺细胞对刀豆蛋白A刺激的增殖能力,ELISA检测胸腺细胞分泌肿瘤坏死因子(TNF)-α、GM-CSF、白细胞介素(IL)-2与IL-6的能力,流式细胞术检测细胞活性氧(ROS)、胸腺细胞凋亡,硫代巴比妥酸法检测丙二醛(MDA),酶学检测超氧化物歧化酶(SOD),DTNB法测定谷胱甘肽(GSH)、氧化谷胱甘肽(GSSG)含量,Western印迹检测细胞衰老相关蛋白p21、p53、Rb的变化。结果 Rg1衰老模型组大鼠胸腺指数升高、胸腺皮质面积比例增加、胸腺细胞的增殖能力提高,凋亡率减少、SA-β-Gal阳性胸腺细胞百分率下降、TNF-α、GM-CSF、IL-2、IL-6的分泌能力明显提高、SOD活性明显提升;ROS和MDA含量下降;p53、p21、Rb蛋白表达有显著下调。结论 D-半乳糖复制的衰老模型大鼠胸腺结构与功能损伤明显,人参皂苷Rg1对其致衰损伤有明确的保护作用,其机制可能与抑制氧化损伤和下调p16-Rb、p53/p21信号通路有关。     

Cellular Retinol-Binding Protein-1 Is Transiently Expressed in Myocardial Infarction Tissue of Rat Model

Objectives To investigate the expression state of cellular retinol-binding protein-1 （ CRBP-1 ） in myocardial infarction （MI） tissue of rat model. Since CRBP-1 is transiently expressed in tissue repairing process, so ventricular remodeling after MI is also a kind of tissue repair, in which we may find the expression of CRBP-1. Methods MI model was produced in male Wistar rats by left coronary ligation. Rats were sacrificed to obtain the heart at 3^rd, 6^th, and 15^th day after operation. Heart was cut into four cross sections, fixed and embedded in paraffin. Sections were cut and stained with hematoxylin and eosin （HE）, Masson＇s trichrome （MT）, rabbit anti-CRBP-1 antibody and mouse anti-a-smooth muscle （SM） actin antibody. CRBP-1 and α-SM actin were also detected using Western blotting. Results Forty-five Wistar rats developed MI with infarct size ranging from 45.6% to 56. 2% （mean 48.6 ± 3.3% ）. Heart sections of MI with HE and MT staining showed a remarkable myocyte necrosis, collagen disposition and ventricular remodeling. CRBP-1 expression was detected at both of the endocardial and epicardial region of infarction, where fibroblasts infiltrated with myocyte necrosis at 3^rd day and 6^th day after operation. At 15^th day, α-SM actin positive fibroblasts in the infarcted region expressed CRBP-1. Conclusions We demonstrate that CRBP-1 is transiently and rapidly expressed by fibrohlast in rat model of MI. Our results therefore indicating a potential relationship between CRBP-1 and ventricular remodeling process after MI.     

Repeated Low-dose of Erythropoietin is Associated with Improved Left Ventricular Function in Rat Acute Myocardial Infarction Model

Objective To evaluate the potential protective affects of Epo on left ventricular (LV) function and remodeling after acute myocardial infarction (MI). Methods Epo was injected into the peritoneum of male Wistar rats (250 g) during 6 weeks post induction of MI. Rats were divided into five groups: MI treated with single high dose (MT1, 5,000 U/kg, n = 10), single high dose (5,000 U/kg) and repeated high doses (MTHi, 1,000 U/kg twice a week; n = 8), or single high dose (5,000 U/kg) and repeated low doses (MTLo, 750 U/kg once a week, n = 10), MI non-treated (MNT, n = 10), sham (S, n = 5). Echocardiography was performed 3.6 ± 1.5 days and 43.7 ± 2.3 days post MI. Collagen deposition and infarct size were measured on histological sections using computerized image analysis. Apoptosis was assessed by ApopTag staining. Results Baseline fractional shortening (FS) was similar between groups. Six weeks after MI the FS of MTLo (26.9%) was significantly higher compared to MNT (17.8%), MT1 (19.5%) and MTH (22.3%) (p = 0.01). However, remodeling indices (end diastolic and end systolic areas, LV circumference) did not improve in the Epo groups, and even worsened in the MTHi group. There was significantly less collagen staining in non-infarct areas in MT1 and MTHi groups compared to MNT and MTLo (0.38 ± 0.3%, 0.49 ± 0.34%, vs 0.89 ± 0.41%, 0.95 ± 0.33%, respectively, p < 0.001). The number of ApopTag positive nucleus was significantly higher in the MNT group compared to the MT1, MTHi, MTLo groups (14.4 ± 8, 7.6 ± 4, 5.8 ± 7, 4.8 ± 5, respectively, p = 0.01 for trend). Conclusion Repeated low doses of Epo after MI improved LV function, but the role of Epo on remodeling is not clear. It did not reduce left ventricular indices, but reduces fibrosis and apoptosis. High Epo doses reduced LV function and aggravated remodeling.     

急性心肌梗死病人左心室重构及心功能的影响因素

目的观察冠心病各种危险因素对急性心肌梗死病人左室重构和心功能的影响.方法 124例急性心肌梗死病人应用超声测定心脏各项指标,分析血压、血脂、吸烟、血尿酸等冠心病危险因素对急性心肌梗死病人左室射血分数(LVEF)的影响,以及高血压对左室重构和功能的影响.结果急性心肌梗死时的收缩压与LVEF值呈明显负相关,收缩压越高,LVEF值越低(P<0.05).其他冠心病危险因素舒张压、血脂、吸烟、血尿酸与LVEF值变化无明显相关性.有高血压病的心肌梗死病人LVEF值明显降低,左室舒张末期内径和左室质量显著高于无高血压病组病人(P<0.001).结论高血压病对急性心肌梗死病人左室重构和心脏功能有明显的影响.     

干细胞移植治疗心肌梗死中长期试验研究现状

干细胞移植治疗心肌梗死是近些年研究的热点,干细胞的种类众多,在治疗心肌梗死上有其各自的特点;据国内外文献报道,干细胞移植治疗心肌梗死的短期疗效安全且肯定,而对中长期疗效的观察正在进行中,现拟对干细胞移植治疗心肌梗死的中长期疗效作一概述。     

Effects of Perindopril on Left Ventricular Remodeling and Osteopontin Expression in Rats With Myocardial Infarction

Objectives To observe the effects of perindopril on left ventricular remodeling and myocardial osteopontin expression in rats with myocardial infarction. Methods In this study male adult SD rats were randomly divided into 3 groups: sham-operation group, MI-saline group and MI-perindopril group. Left anterior descending artery was ligated to generate myocardial infarction. Perindopril (2 mg/kg body weight/day) was administered from the next day of MI. Four weeks later, left ventricular diameter (LVEDD and LVESD) and left ventricular ejection fraction was estimated with echocardiography, LVSP, LVEDP and±dp/dtmax was detected with hemodynamic measurement, cardiomyocyte diameter and interstitial fibrosis infiltration were evaluated with histological methods, and myocardium osteopontin protein expression level was detected with western blot. Results ①Compared with the sham-operation group, all rats with MI developed significant systolic and diastolic dysfunction, as was indicated by decreased LVEF, LVSP and±dp/dtmax, as well as increased LVEDP. ②Rats with MI showed significantly dilated left ventricles and higher ventricular weight / body weight ratio, significantly increased cardiomyocyte diameter and marked interstitial fibrosis in the non-infarction area. ③Perindopril treatment partly prevented cardiac dysfunction and left ventricular remodeling as indicated by the parameters mentioned above. ④No osteopontin protein was detected in myocardium of sham-operation rats. In rats with MI, high level osteopontin protein expression was significantly inhibited by perindopril treatment. Conclusions In rats with MI, perindopril treatment significantly prevented left ventricular remodeling and myocardium osteopontin protein expression.     

Simvastatin Regulates Myocardial Cytokine Expression and Improves Ventricular Remodeling in Rats after Acute Myocardial Infarction

Purpose: Studies have showed that inflammatory cytokines were involved in the process of left ventricular (LV) remodeling after acute myocardial infarction (AMI), anti-inflammation treatment ameliorated LV remodeling and improved cardiac performance. Hydroxymethylglutary coenzyme A reductase inhibition (statins) could affect the expression of inflammatory cytokines. We hypothesized that statins have beneficial effects on early LV remodeling and cardiac performance in rats with AMI by modulating the production of inflammatory cytokines.Methods: Rats with AMI were treated with placebo or simvastatin (gastric gavage) for 4 weeks. The pro-inflammatory cytokines: tumor necrosis factor (TNF)-, interleukin (IL)-1, IL-6 and the anti-inflammatory cytokine: IL-10 excreted by cardiac myocytes was examined. Echocardiography, hemodynamics and collagen type I production were measured to evaluate LV remodeling and cardiac function.Results: The mRNA expression and protein production of TNF-, IL-1, IL-6 and IL-10 in AMI group were significantly elevated compared with sham rats. Simvastatin markedly attenuated the production of TNF-, IL-1, IL-6 and increased IL-10 levels in the noninfarcted and infarcted regions, reduced collagen deposition in the noninfarcted myocardium and improved left ventricular function. However simvastatin did not alter plasma lipids.Conclusions: Simvastatin ameliorates early LV remodeling and improve cardiac function after AMI. Simultaneously, it decreased pro-inflammatory and increased anti-inflammatory cytokines, which suggests, but does not prove, a causal relationship independent of plasma lipid-lowering effects.Jinying Zhang and Xiang Cheng contribute to the work equally.This study was supported by grants from National Natural Science Foundation of China (No. 30370574).