围术期应用粒细胞集落刺激因子对大鼠心脏术后心功能的影响

目的 探讨围术期应用粒细胞集落刺激因子(G-CSF)对大鼠心脏术后心功能的影响.方法 将Wistar雄性大鼠随机分为3组,每组10只,暴露心脏后于左心室沿冠状动脉左前降支附近作一切口后立即缝合切口并关胸.对照组不使用G-CSF,仅完成手术过程;G-CSF预处理组术前通过鼠尾静脉注射G-CSF 5 d；G-CSF预处理+心内注射组除术前通过鼠尾静脉注射G-CSF 5 d外,手术过程中将G-CSF直接注射在心室切口周围.术后第7、28天行超声心动图检查评价心脏结构和心功能.结果 第7大时,对照组左心室射血分数(LVEF)和缩短分数(FS)分别为(52.8±2.9)％、(22.2±1.4)％,G-CSF预处理组和G-CSF预处理+心内注射组LVEF[分别为(56.5±4.3)％、(61.2±3.6)％]、FS[分别为(25.2±2.5)％、(29.5±2.3)％]均明显高于对照组,差异有统计学意义(均P＜0.05);G-CSF预处理组和G-CSF预处理+心内注射组左心室收缩末内径(LVESD)[分别为(6.25±0.92)、(5.51±0.85)mm]和左心室收缩末容量(LVESV)[分别为(0.57±0.18)、(0.44±0.14)ml]低于对照组[分别为(6.60±1.10)mm、(0.67±0.31)ml],G-CSF预处理+心内注射组LVESD和LVESV低于G-CSF预处理组,差异均有统计学意义(均P＜0.05).第28大时G-CSF预处理组和G-CSF预处理+心内注射组的LVEF[分别为(59.6±4.7)％、(63.8±1.9)％]和FS[分别为(26.2±2.8)％、(30.9±1.6)％]均明显高于对照组[分别为(53.4±3.6)％、(23.6±1.7)％],LV ESD[分别为(5.92±0.72)、(5.35±0.54)mm]、左心室舒张末内径(LVEDD)[分别为(7.48±0.61)、(7.26 ±0.55)mm] 、LVESV [分别为(0.49±0.14)、(0.41±0.08)m1]、左心室舒张末容量(LVEDV)[分别为(1.05±0.25)、(1.02±0.27)ml]低于对照组[分别为(6.98±0.37)mm、(8.04±0.42)mm、(0.76±0.15)ml、(1.37±0.18)ml],差异均有统计学意义(均P＜0.05);G-CSF预处理+心内注射组LVEF、FS明显高于G-CSF预处理组,LVESD、LVEDD、LVESV、LVEDV明显低于G-CSF预处理组,差异均有统计学意义(均P＜0.05).结论 围术期应用G-CSF可明显改善大鼠心脏术后心脏收缩及舒张功能.     

辛伐他汀对大鼠心肌梗死后心室重塑影响的实验研究

目的探讨辛伐他汀对大鼠心肌梗死后心脏功能和心室重塑的影响。方法结扎大鼠冠状动脉前降支建立心肌梗死模型,24 h后存活大鼠随机分成心肌梗死组(M I组)、辛伐他汀20 mg组(20 mg.kg-1.d-1)和40 mg组(40 mg.kg-1.d-1),另单设假手术组(Sham组)。8 wk后测定血液动力学指标,血清血脂水平,心室重量指数,苦味酸天狼猩红染色后观察心脏形态学改变,测定心肌胶原容积分数。结果各组血脂水平无统计学差异;MI组心室重量指数增加,心脏收缩及舒张功能受损,梗死边缘区胶原沉积明显,胶原比例改变。两个辛伐他汀(simvastatin,Sim)组均能减轻心室重量指数,改善心脏功能,减少梗死边缘区胶原沉积。结论辛伐他汀能抑制心肌梗死后心室重塑,其机制可能与抑制心肌梗死后心肌肥大和心肌间质纤维化相关,而与其降脂作用关系不大。     

大豆异黄酮对心肌梗死大鼠心室重构的影响(英文)

目的：观察大豆异黄酮对心肌梗死大鼠心室重构的影响。方法：雄性SD大鼠,结扎冠状动脉左前降支,造成心肌梗死。实验分为6组：假手术组,心肌梗死模型组,卡托普利组,大豆异黄酮低、中、高剂量组。在结扎冠状动脉后3h开始,分别灌胃给予0.5%羧甲基纤维素钠(CMC-Na),0.5%CMC-Na,卡托普利50mg·kg~(-1)和大豆异黄酮30,90,270 mg·kg~(-1),qd,共35 d。给药容积均为10 mL·kg~(-1)。最后一次给药后24 h,测定心率(HR)、左室舒张末期压(LVEDP)、左室收缩压峰值(Peak)、左室压最大上升速率/下降速率(±dp/dt_(max))和心肌最大缩短速率(V_(max)),测定全心室质量和体重比(TVW/BW),用天狼猩红染色,在图像分析系统下测量梗死范围(IS)、左心室内径(LVD)、室间隔厚度(ST),心肌间质胶原容积系数(ICVF)和血管周围胶原容积系数(PCVF)。结果：卡托普利、大豆异黄酮90 mg·kg~(-1)和270 mg·kg~(-1)组大鼠的梗死范围分别是(31±s4)%,(32±3)%和(31±5)%,均显著小于心肌梗死模型组大鼠[(38.9±2.9)%,P＜0.01]。心肌梗死组大鼠的TVW/BW,LVD,ICVF和PCVF均比假手术组明显增加(P＜0.01),增加的TVW/BW,LVD,ICVF和PCVF用卡托普利和大豆异黄酮90 mg·kg~(-1),270 mg·kg~(-1)治疗后明显减少[P＜0.01,P＜0.05(SI 90 mg·kg~(-1)组的LVD)]。心肌梗死大鼠的ST显著减小(P＜0.01),而给予卡托普利和大豆异黄酮可增加ST(P＜0.01)。结扎LAD后,大鼠的Peak,±dp/dt_(max)和V_(max)明显降低(P＜0.01),而LVEDP明显升高(P＜0.01),降低的Peak,±dp/dt_(max)和V_(max)在给予卡托普利、大豆异黄酮90 mg·kg~(-1)和270 mg·kg~(-1)后明显升高(P＜0.01)；而升高的LVEDP仅在给予卡托普利治疗后降低。结论：大豆异黄酮能够改善心肌梗死大鼠的心功能和心室重构。     

补肾活血方对大鼠心肌梗塞后心肌纤维化干预作用的实验研究

目的:观察补肾活血方对大鼠心肌梗塞(MI)后左室心肌纤维化(MF)的干预作用。方法:结扎左冠状动脉前降支建立大鼠心肌梗塞模型,随机分为模型组、阳性药物组、补肾活血方高剂量组(10 g生药.kg-1)、中剂量组(5 g生药.kg-1)和低剂量组(2.5 g生药.kg-1)。于造模当天连续给药14 d后测定各组大鼠心脏重量指数、梗死面积、HE染色观察组织病理学变化、Masson染色法观察心肌胶原纤维的表达,免疫组织化学观察心肌组织非梗死区Ⅰ、Ⅲ型胶原的表达。结果:各组大鼠的心脏重量指数及梗死面积无统计学差异;HE染色提示阳性药物依那普利和补肾活血方高、中、低组均可在一定程度上减轻心肌梗塞后组织的病理学改变,炎性细胞浸润得到较好缓解;Masson染色提示阳性药物依那普利和补肾活血方高、中、低组心肌间质纤维化程度减轻;I型、III型胶原的免疫组化染色提示:与模型组相比,各组均可在一定程度上降低非梗死区Ⅰ型胶原和Ⅲ型胶原的表达量(P<0.01);与补肾活血方低剂量组比较,高、中剂量组非梗死区Ⅰ和Ⅲ型胶原的表达量均有显著统计学差异(P<0.01);高、中剂量组间无统计学差异。结论:补肾活血方可通过抑制非梗死区I型、III型胶原纤维的合成,减轻梗死后心肌纤维化程度。     

卡维地洛对大鼠急性心肌梗死后非梗死区胶原重塑的影响

目的卡维地洛对大鼠急性心肌梗死（AMI）后非梗死区胶原重塑的影响。方法冠状动脉结扎术后24h存活的雌性SD大鼠83只，完全随机分为心肌梗死组43例和卡维地洛组40例，另设假手术组27例；各组按观察时间48h和4周再分为：心肌梗死48h组和心肌梗死4周组，卡维地洛48h组和卡维地洛4周组，假手术48h组和假手术4周组。免疫组织化学方法检测心肌胶元-Ⅰ、胶元-Ⅲ的胶原容积分数（CVF）。结果①与假手术48h组相比心肌梗死48h组的主动脉收缩压（SBP）、舒张压（DBP）和平均动脉压（MAP）、左心室收缩压（LVSP）和左心室内压最大上升和下降速率（±dp／dt）均降低，差异有统计学意义（P〈0．05或P〈0．01），左心室舒张末压（LVEDP）则显著升高[（6，064-4．64）对比（1．314-2．67），P〈0．05]；②与假手术4周组比，心肌梗死4周组仅LVSP、±dp／dt和心率均降低，差异有统计学意义（P〈0．05或P〈0．01），LVEDP甚至比心肌梗死48h组更高[（19．86±12．76）对比（6．06±4．64），P〈0．01]，同时Collagen—Ⅰ、Collagen—Ⅲ的CVF升高，差异有统计学意义（P〈0．05）；③与心肌梗死48h组相比，卡维地洛48h组的LVSP、±dp／dt和心率均降低，差异有统计学意义（P〈0.05或P〈0．01），但LVEDP无显著变化。与心肌梗死48h组相比，卡维地洛4周组的LVEDP[（11．93±9.79）对比（19．86±12．76）]、Collagen—Ⅰ、Collagen—Ⅲ的CVF[（3．82±1．16）对比（8．10±1．77）；（2．67±0．82）对比（5．26±1．87）]均降低，差异有统计学意义（P〈0．05或P〈0．01），但LVSP、±dp／dt均无显著变化。结论AMI后，发生血流动力学和左心室功能异常，非梗死区胶原-Ⅰ、Ⅲ含量均增加。卡维地洛4周能有效降低AMI后大鼠左心室舒张末压。改善血流动力学和左心功能。卡雏地洛治疗对AMI后大鼠非梗死区Ⅰ-型、Ⅲ-型胶     

Granulocyte colony-stimulating factor reduces mortality by suppressing ventricular arrhythmias in acute phase of myocardial infarction in rats

Our aim was to evaluate the effects of granulocyte colony-stimulating factor (G-CSF) on early cardiac arrhythmias after myocardial infarction (MI) and the impact on survival. Male Wistar rats received repeated doses of 50 mug/kg G-CSF (MI-GCSF group) or vehicle (MI group) at 7, 3, and 1 days before surgery. MI was induced by permanent occlusion of left coronary artery. The electrocardiogram was obtained before occlusion and then for 30 minutes after surgery. Events and duration of ventricular arrhythmias were analyzed. The levels of connexin43 (Cx43) were measured by Western blot immediately before MI production. Survival was significantly increased in MI-GCSF pretreated group (74% versus 52.9% MI, P < 0.05). G-CSF pretreatment also significantly reduced the ventricular premature beats when compared with the untreated-MI group (201 +/- 47 versus 679 +/- 117, P < 0.05). The number and the duration of ventricular tachycardia were smaller in the MI-G-CSF group, as well as the number of ventricular fibrillation episodes (10% versus 69% in MI, P < 0.05). Cx43 levels were significantly increased by G-CSF treatment (1.27 +/- 0.13 versus 0.86 +/- 0.11; P < 0.05). The MI size 24 hours after occlusion was reduced by G-CSF pretreatment (36 +/- 3% versus 44 +/- 2% of left ventricle in MI group; P < 0.05). The increase of Cx43 expression in the heart may explain the reduced incidence in ventricular arrhythmias in the early phases after coronary artery occlusion in rats, thus increasing survival after MI.     

机械加载可改善心肌梗死大鼠的心肌损伤

摘要：目的 探讨机械加载对心肌梗死大鼠心肌损伤的改善作用。方法 选用8周龄Wistar雄性大鼠30只,体 质量约200 g,按随机数字表法分为假手术对照组（Sham组）、心肌梗死组（MI组）和心肌梗死机械加载治疗组（MI+L 组）,每组10只,心肌梗死建模后1 d开始膝关节机械加载治疗2周。检测治疗后大鼠心电图Ⅱ导联ST段、心脏质量 指数（HMI）、左心室质量指数（LVMI）、心脏质量/胫骨长度,2,3,5－三苯基氯化四氮唑（TTC）染色检测左室舒张末内 径（LVEDD）和梗死范围;HE染色检测炎性细胞数;Masson染色检测胶原容积分数（CVF）;免疫组织化学染色检测核 因子（NF）-κB p65亚基、白细胞介素（IL）-6和基质金属蛋白酶（MMP）-9蛋白的表达。结果 与Sham组相比,心肌 梗死导致MI组心电图Ⅱ导联ST段抬高,HMI、LVMI、LVEDD、心脏质量/胫骨长度和梗死范围明显增加;机械加载治 疗后,MI+L组Ⅱ导联ST段抬高幅度下降,HMI、LVMI、LVEDD、心脏质量/胫骨长度和梗死范围较MI组明显降低（P＜ 0.05）。心脏组织学结果表明,心肌梗死导致炎性细胞数和CVF增加,通过加载治疗后,炎性细胞数和CVF明显改善 （P＜0.05）。免疫组化染色结果表明,心肌梗死导致大鼠心肌NF-κB p65、IL-6和MMP-9蛋白表达升高,机械加载能 够抑制3种蛋白的表达。相关性分析结果表明,NF-κB p65、IL-6和MMP-9三者之间表达呈正相关,三者与心室重构 指标（LVEDD、HMI、LVMI和心脏质量/胫骨长度）呈正相关。结论 机械加载可以明显改善心肌梗死大鼠心肌损伤, 该治疗作用可能与机械加载减轻心肌梗死后炎症反应和抑制心室重构有关。     

辛伐他汀对心肌梗死后大鼠左室重构及心肌β3整合素表达的影响

目的研究辛伐他汀对心肌梗死后4wk雄性SD大鼠心功能、左室质量指数、心肌组织β3整合素及Ⅰ型胶原表达的影响。方法冠脉结扎后24h存活的大鼠随机分2组:辛伐他汀组(辛伐他汀30mg·kg~(-1)·d~(-1)灌胃,n=14)和模型组(等量生理盐水灌胃,n=14)。另设假手术组(Sham组,等量生理盐水灌胃,n=9),治疗4wk。结果模型组左室质量指数(2.53±s 0.14)mg·g~(-1)及左室舒张末压(13.9±1.3)mmHg均高于Sham组(P<0.01);辛伐他汀组分别为(2.24±0.08)mg·g~(-1)和(5.6±3.6)mmHg,低于模型组(P<0.01)。模型组胶原容积分数为(12.6±3_3)%,较Sham组增加(P<0.01);辛伐他汀组为(5.6±0.5)%,低于模型组(P<0.01)。模型组β3整合素和Ⅰ型胶原表达较Sham组增多(P<0.01),而辛伐他汀组低于模型组(P<0.01)。结论辛伐他汀可改善心肌梗死后心功能和左室重构,其机制之一可能是抑制β3整合素表达。     

粒细胞巨噬细胞集落刺激因子与乙型肝炎疫苗协同诱导的特异性免疫应答

目的考察粒细胞巨噬细胞集落刺激因子(Gm-csf)对乙型肝炎疫苗免疫原性及诱导的体液免疫效果的加强作用。方法将Gm-csf和乙肝疫苗分别采用4种不同的免疫顺序,联合免疫BALB/c小鼠。定期用酶联免疫吸附法检测小鼠产生的抗乙型肝炎表面抗原(抗-HBsAg)的抗体水平。结果联合免疫Gm-csf,可提高小鼠产生的抗-HBsAg抗体水平;②单次免疫后7 d,混合疫苗组的血清抗体滴度最高,为疫苗组的7.5倍;直至免疫后35 d,混合疫苗组仍为最高,为疫苗组的9.2倍;③二次免疫后14 d,混合疫苗组血清中抗体滴度与疫苗组相比有显著性提高(P<0.05),随后GM+疫苗组、混合疫苗组和疫苗+GM组血清中抗体滴度都先后达到峰值,分别为疫苗组的10.0,10.1,8.2倍。④小鼠血清中抗体水平达到稳定状态后,用乙肝疫苗原液进行挑战实验,抗体快速达到峰值,分别为挑战实验前的9.2,5.2,12.8,4.8倍。结论通过Gm-csf的联合免疫,可提高乙型肝炎疫苗的免疫原性,增强乙型肝炎疫苗诱导的体液免疫水平。     

粒细胞集落刺激因子对脂肪基质细胞增殖的影响

目的 探讨粒细胞集落刺激因子(G-CSF)对大鼠脂肪基质细胞(ADASc)增殖的影响.方法 将16只SD大鼠随机分为两组,即G-CSF组(8只)与对照组(8只).G-CSF组皮下注射G-CSF 20μg·kg-1·d-1,连用5 d;对照组皮下注射等量0.9%氯化钠注射液.每组分别于最后一次注射后6 h取大鼠腹膜后脂肪组织,分离、培养、鉴定ADASc,取两组第5代的ADASc,观测细胞生长的最大增殖倍数和倍增时间,流式细胞仪测定细胞周期分布.结果 差异贴壁法培养出的第5代ADASc细胞为高纯度细胞群,表型特征为CD44+CD105-CD31-CD45-.G-CSF组与对照组大鼠ADASc最大增殖倍数、倍增时间、细胞周期Go-1细胞比例差异有统计学意义(P<0.05).G-CSF组大鼠ADASc与对照组比较,具有更大的增殖倍数和更短的倍增时间,处于Go-1周期的细胞数目也相对要少.结论 差异贴壁法是培养ADASc一种比较好的方法;G-CSF可促进骨髓ADASc进入细胞增殖周期.     

粒细胞巨噬细胞集落刺激因子与乙肝疫苗协同诱导小鼠细胞免疫应答

目的考察粒细胞巨噬细胞集落刺激因子(Gm-csf)对乙型肝炎疫苗免疫原性及诱导的细胞免疫效果的加强作用。方法将Gm-csf和乙型肝炎疫苗分别采用4种不同方式免疫BALB/c小鼠,免疫后,制备脾细胞,再以相应的HBsAg体外刺激,酶联免疫法(ELISA)测定细胞因子分泌水平,MTT法测定脾细胞对抗原刺激指数;以YAC-1细胞为靶细胞,测定细胞毒性T淋巴细胞活性;同时ELISA法测定血清中特异性抗体IgG1和IgG2a。结果GM+疫苗组小鼠脾细胞产生的IFN-γ水平最高,显著高于其它组(P<0.05),而各免疫组IL-5水平没有显著差别(P>0.05);GM+疫苗组小鼠脾细胞对抗原刺激的刺激指数显著高于其它各组(P<0.05);GM+疫苗组小鼠脾细胞对YCA-1的杀伤性显著高于其它各组(P<0.01)。结论通过Gm-csf的联合免疫,可提高乙型肝炎疫苗的免疫原性,增强乙型肝炎疫苗诱导的细胞免疫水平。     

Relationship between endogenous colony stimulating factors and apoptosis in human colon cancer cells: role of cyclo-oxygenase inhibitors.

1. Nonsteroidal anti-inflammatory drug (NSAID) usage is associated with gastrointestinal inflammatory damage and aggravation of gut inflammatory conditions. NSAIDs also exert a preventive effect against colon cancer that seems to be due to increased colon cell apoptosis. NSAIDs have been shown to modulate the release of colony stimulating factors (CSFs) in some cells. In the present study we analysed the effect of these drugs on secretion of CSFs and apoptosis in human colon epithelial cells (HT-29). 2. HT-29 cells secreted bioactive levels of GM-CSF, G-CSF and M-CSF when stimulated with IL-1ss and TNF-alpha, and diclofenac (10(-7)-10(-4) M), indomethacin (10(-7)-10(-4) M) and sodium salicylate (10(-5)-10(-2) M) induced concentration-dependent increases in GM-CSF secretion. 3. Reduced secretion of G-CSF and M-CSF and increased cell apoptosis were observed with the highest concentrations of these non-selective NSAIDs. 4. No changes in any CSF release or HT-29 cell apoptosis were detected in the presence of the COX-2 selective inhibitor DFP (10(-7)-10(-4) M). 5. Neither the exogenous addition of CSFs nor the blockade of secreted CSFs modified apoptosis in HT-29 cells stimulated with cytokines and/or NSAIDs. 6. These results suggest that colon epithelial cells can contribute to local inflammatory responses by releasing CSFs and thus extend the life span of local leukocytes. Modulation of CSF levels by non-selective NSAIDs may be involved in the pro-inflammatory effects of these agents in the gut.     

Cardioprotective effects of granulocyte colony-stimulating factor in angiotensin II-induced cardiac remodelling

1. Granulocyte colony stimulating factor (G-CSF) is reported to have a beneficial effect on cardiac dysfunction in postinfarction and doxorubicin-induced cardiomyopathy. Thus, the aim of the present study was to investigate the effects of G-CSF on cardiac remodelling in angiotensin (Ang) II-induced hypertrophy. 2. Four groups of mice were investigated. The first group served as a control group. The second group was injected with recombinant human G-CSF (10 microg/kg per day, s.c.) on the first 5 days of each week and treatment was continued for 4 weeks. An osmotic minipump was implanted subcutaneously into each mouse in the third group so that pressor doses of AngII (2.88 mg/kg per day) or saline could be administered over a period of 4 weeks. The fourth group was infused with AngII (2.88 mg/kg per day) and injected with G-CSF (10 microg/kg per day, s.c.) for 4 weeks. 3. Angiotensin II treatment significantly elevated blood pressure and caused cardiac hypertrophy and fibrosis in mice. Treatment of mice with G-CSF did not reduce the AngII-induced increase in blood pressure, but ameliorated the development of cardiac fibrosis and hypertrophy. Infusion of AngII induced upregulation of angiotensin-converting enzyme (ACE) expression and downregulation of ACE2 expression. Treatment with G-CSF reduced cardiac levels of ACE and increased ACE2 expression. In addition, G-CSF treatment reduced the expression of osteopontin (OPN) and phospho-p70S6 kinase, which were upregulated by AngII infusion. 4. These results suggest that G-CSF reduces AngII-induced hypertrophy. Modulation of the expression of the ACE isoforms contributes to regression of AngII-induced cardiac hypertrophy. The effect of G-CSF to prevent cardiac fibrosis and hypertrophy may be mediated, in part, via inhibition of OPN expression and p70S6 kinase phosphorylation.     

基因重组人粒细胞集落刺激因子防治肺癌化疗反应

目的 :探讨国产基因重组人粒细胞集落刺激因子 (rHuG CSF)对肺癌病人化疗所致白细胞减少的防治作用及不良反应。方法 :采用随机分组、自身交叉对比的方法 ,将 6 0例肺癌VIP方案化疗病人分成A ,B两组 (各 30例 ) ,A组第 1周期化疗结束 4 8h开始皮下注射rHuG CSF 3μg·kg- 1,qd ,7～14d ,第 2周期单用化疗 ;B组第 1周期单用化疗 ,第 2周期化疗结束 4 8h开始皮下注射rHuG CSF 3μg·kg- 1,qd ,7～ 14d。自化疗开始隔日查血常规 1次 ,观察白细胞及中性粒细胞的变化。结果 :治疗周期白细胞总数及中性粒细胞最低值均高于对照周期 ,最低值的持续时间和化疗开始至细胞恢复到正常值以上的时间均少于对照周期。骨痛、肌痛和乏力发生率分别为 10 %和 7% ,偶有发热。结论 :rHuG CSF对化疗引起的白细胞减少具有预防和治疗作用 ,不良反应轻微 ,安全可靠。     

Comparison of cardioprotective effects of mibefradil and ramipril in stroke-prone spontaneously hypertensive rats

INTRODUCTION Acutemyocardial infarction(MI), particularlylargeand transmural infarctions, can result in complex alter-ations of cardiac architecture involving both the inf-used in the treatment of clinical myocardial ischemia. GmbH, Soest, Germany) and tap water. The investiga-However, their therapeutic properties in myocardial in- tion was under the Guide for the Care and Use of Labo-farction-induced heart failure is not clearly defined. rat…     

麝香合剂对大鼠急性心肌梗死的影响(英文)

目的:观察麝香合剂对急性心肌梗死大鼠梗死范围、血清肌酸磷酸激酶(CPK)和乳酸脱氢酶(LDH)活力以及血流动力学的影响。方法:雄性SD大鼠随机分为6组,假手术组,心肌梗死组,麝香合剂3.8,7.6,15.2pill·kg-1组和麝香保心丸0.6pill·kg-1组,分别灌胃给予0.5%羧甲纤维素钠(CMCNa),0.5%CMCNa,3种浓度麝香合剂混悬液,麝香保心丸混悬液,每日给药1次,连续给药3d,给药容积为10mL·kg-1。最后1次给药后30min,结扎冠状动脉左前降支(LAD)制备心肌梗死模型。冠状动脉结扎后24h,测量大鼠的梗死范围、血清CPK和LDH活力以及血流动力学参数。结果:麝香合剂7.6,15.2pill·kg-1组和麝香保心丸组大鼠的梗死范围分别是(15.2±2.4)%,(13.±2.0)%和(18±3)%,均显著小于心肌梗死组大鼠[(21.9±2.0)%,P<0.01]。心肌梗死组大鼠的血清CPK和LDH活力均明显高于假手术组(P<0.05,P<0.01),而升高的酶活力可以被预先给予麝香合剂或麝香保心丸所降低(P<0.05P<0.01)。心肌梗死组大鼠的动脉收缩压(SBP)动脉舒张压(DBP)、左室收缩压峰值(Peak)、左室压最大上升速率/下降速率(±dp/dtmax)和心肌最大缩短速率(Vmax)明显降低(P<0.05,P<0.01),而左室舒张末期压(LVEDP)明显升高(P<0.01)。预先给予麝香合剂7.6,15.2pill·kg-1和麝香保心丸可使降低的+d     

Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats

Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries.     

粒细胞巨噬细胞集落刺激因子与三种不同来源的乙肝疫苗协同诱导的特异性免疫应答的比较

目的比较粒细胞巨噬细胞集落刺激因子(Gm-csf)对三种不同来源的乙肝疫苗免疫原性及诱导的体液免疫效果的加强作用。方法将重组Gm-csf和三种不同来源的乙肝疫苗分别按相同程序,联合免疫小鼠,定期用酶联免疫吸附法检测小鼠产生的抗乙型肝炎表面抗原(抗-HBsAg)的抗体水平。结果免疫1周后,CHO细胞疫苗组、汉逊酵母疫苗组、啤酒酵母疫苗组血清中抗-HBsAg抗体阳性率分别为90%,10%,0%;免疫2周后分别为100%,40%,40%;二次免疫后,三个实验组小鼠血清中抗体持续增加。结论通过Gm-csf的联合免疫,可提高乙型肝炎疫苗的免疫原性,增强乙型肝炎疫苗诱导的体液免疫水平。