MAPK信号通路介导CT-1促进大鼠心肌细胞存活

目的探讨心脏营养素-1(CT-1)对培养乳鼠心肌细胞存活的促进作用以及丝裂原激活蛋白激酶(MAPK)信号传导途径在CT-1促进心肌细胞存活中的作用。方法差速贴壁纯化培养新生大鼠心肌细胞,MTT比色法测定各孔细胞存活率。结果无血清DMEM培养心肌细胞24 h后,加入4个剂量组CT-1(10-10~10-7mol/L),呈明显剂量依赖性增加MTT计数;培养基中加入CT-1(10-8mol/L),1、2、3和4 d MTT计数呈明显的时间依赖性增加;预先用MAPK抑制剂PD098059(5×10-5mol/L),再加入CT-1,心肌细胞存活率明显低于单纯CT-1组,而单纯用PD098059则无明显影响;预先用PKC激动剂PMA(10-5mol/L),再加入CT-1,MTT计数明显增加;先用PD098059,再加入PMA和CT-1,MTT计数明显降低,而先用PKC抑制剂Calphostin C(Cal)再加CT-1,MTT计数也明显降低。结论CT-1增加心肌细胞存活率的效应是由MAPK信号分子介导实现的;该效应的胞内信号传导通路可能是先激活PKC信号分子,然后再激活MAPK信号分子。     

如何利用Blackboard教学管理系统构建生理学网络课程

B lackboard教学管理系统可为教师创建、发布和管理网络课程提供方便、快捷的工具模块。文章介绍了如何利用B lackboard教学管理系统提供的课程内容模块、测验模块和课程工具模块来构建生理学网络课程的过程。指出生理学网络课程的建设,对突破传统面授教学的局限性和帮助学生网上学习具有重要意义。     

siRNA沉默HIF-1α对大鼠心肌细胞CT-1表达的影响

目的 研究低氧诱导因子-1α(HIF-1 α)在心肌细胞适应低氧环境中作用机制.方法 合成针对HIF-1α的siRNA片段,转染大鼠心肌细胞系H9C2.Real-time PCR检测HIF-1α和心肌营养素(CT-1) mRNA水平,Westernblot检测HIF-1α和CT-1蛋白水平.结果 低氧环境下,转染针对HIF-1α siRNA片段后HIF-1α mRNA水平、HIF-1 α蛋白质水平、CT-1 mRNA水平和蛋白水平均明显减低(P＜0.05).不进行转染时,CT-1 mRNA水平、HIF-1α蛋白和CT-1蛋白水平在低氧下比常氧下明显增高(P＜0.05).CT-1蛋白由对照组的0.34 ±0.05增至0.55 ±0.05(P＜0.05).结论 低氧情况下CT-1基因的调控作用有可能是通过低氧激活HIF-1α而诱导产生的,HIF-1α在心肌细胞适应低氧环境中具有重要作用.     

补肾降脂方对高脂血症脂肪性肝炎治疗作用的实验研究

目的:研究补肾降脂方在脂质肝损伤的作用.方法:把SD大鼠随机分为5组,除空白对照组外均饲以高脂饲料造模,连续喂养8周.用补肾降脂方给予治疗,并与阳性对照药舒降之组对比,用药2周后取血,取肝,以备检测.结果:补肾降脂方组血浆LPL、HL活性降低,肝组织病理切片显示补肾降脂方组能明显改善细胞变性程度,细胞凋亡数目减少.结论:补肾降脂方可以降低脂质在肝脏中的沉积,保护肝组织,对脂肪性肝炎有治疗作用.     

电刺激兔小脑顶核对血压和血浆心钠素的影响

目的　探讨小脑顶核加压反应是否有体液因素的参与以及孤束核在其中的作用。　方法　利用电刺激小脑顶核引起血压变化的同时 ,观察血浆心钠素的变化。在此基础上电损毁孤束核后 ,观察刺激顶核的上述作用有无变化。　结果　电刺激小脑顶核后动脉收缩压和舒张压分别为 (2 0 .5 6± 2 .99)KPa和 (14 .16± 2 .71)KPa ,明显高于刺激前的 (14 .97± 2 .69)KPa和 (9.96± 2 .4)KPa(P <0 .0 1) ,而血浆心钠素则为 (160 1.61± 2 90 .69)Pmol/L明显低于刺激前的 (2 3 3 3 .79± 44 7.47)Pmol/L(P <0 .0 5 ) ;电损毁孤束核后电刺激小脑顶核 ,动脉血压、血浆心钠素 ,皆无明显变化 (P>0 .0 5 )。　结论　心钠素参与顶核加压反应的调节 ,孤束核可能中介顶核加压反应。     

校外与校内生理学考题质量分析

为了实行考教分离，提高教学质量，我院从９４级本科班开始使用校外题（大多数为部属医科大学的考题），对本科生进行期末考试。９４级本科班生理学期末考试采用的是湖南医科大学的生理学试题。两年后由于教研室建立了自己的题库，９６级本科班生理学期末考试则应用校内题...     

在模拟低氧环境下心肌细胞HIF-1与CT-1的相互作用

目的:研究低氧环境下大鼠心肌细胞系H9C2细胞中HIF-1与CT-1的相互作用。方法:氯化钴(CoCl2)模拟低氧环境。采用CCK-8试剂盒检测心肌细胞存活率。化学合成siRNA片段,并通过li-pofectamine 2 000转染大鼠心肌细胞系H9C2。采用Real-time PCR和Western-blot技术分别检测HIF-1α和CT-1的mRNA和蛋白质水平。结果:低氧处理48h后,干扰组(转染针对HIF-1α的siR-NA的H9C2)中CT-1mRNA和蛋白水平较对照组(转染无义干扰片段的H9C2)明显减少(P<0.05)。低氧3d和4d后,加入CT-1组的心肌细胞存活率较对照组高(P<0.05),HIF-1mRNA表达水平与对照组无显著差异(P>0.05),HIF-1蛋白水平增加。结论:在培养心肌细胞中模拟低氧环境,HIF-1表达减少伴随着CT-1表达减少,加入CT-1后,HIF-1蛋白表达也增加,HIF-1与CT-1相互作用。     

利用Visual Foxpro 6.0开发生理学试题库管理系统

为了提高教学管理水平 ,进一步保证教学质量 ,实现考试命题的电脑化、随机化、自动化 ,减轻手工命题的重复劳动 ,我们以全国本科、专科规划教材为基础 ,参考多种国内外生理学教材和试题选编 (试题集 )建立了生理学试题库 ,其中包括名词解释、是非判断、填空题、单项选择、问答题五种题型。并利用 Visual Foxpro6 .0开发了《生理学试题库管理系统 TKGL 2 .0版》,经近一年的运行使用 ,取得了预期的效果。现将设计开发过程介绍如下。1　系统功能设计本系统由试题库维护、试题查询、试题组卷、试卷保存、帮助信息五个基本模块组成。其主要功…     

CT-1-CP-induced Ventricular Electrical Remodeling in Mice

The chronic effects of carboxyl-terminal polypeptide of Cardiotrophin-1(CT-1-CP) on ventricular electrical remodeling were investigated. CT-1-CP, which contains 16 amino acids in sequence of the C-terminal of Cardiotrophin-1, was selected and synthesized, and then administered to Kunming mice(aged 5 weeks) by intraperitoneal injection(500 ng·g-1·day-1)(4 groups, n=10 and female: male=1:1 in each group) for 1, 2, 3 and 4 weeks, respectively. The control group(n=10, female:male=1:1) was injected by physiological saline for 4 weeks. The epicardial monophasic action potential(MAP) was recorded by using a contact-type MAP electrode placed vertically on the left ventricular(LV) epicardium surface, and the electrocardiogram(ECG) signal in lead Ⅱ was monitored synchronously. ECG intervals(RR, PR, QRS and QT) and the amplitude of MAP(Am), the maximum upstroke velocity(Vmax), as well as action potential durations(APDs) at different repolarization levels(APD30, APD50, APD70, and APD90) of MAP were determined and analyzed in detail. There were no significant differences in RR and P intervals between CT-1-CP-treated groups and control group, but the PR segment and the QRS complex were greater in the former than in the latter(F=2.681 and 5.462 respectively, P<0.05). Though QT interval and the corrected QT interval(QTc) were shorter in CT-1-CP-treated groups than in control group, the QT dispersion(QTd) of them was greater in the latter than in the former(F=3.090, P<0.05) and increased with the time. The ECG monitoring synchronously with the MAP showed that the compression of MAP electrode on the left ventricular epicardium induced performance similar to myocardium ischemia. As compared with those before chest-opening, the PR segment and QT intervals remained basically unchanged in control group, but prolonged significantly in all CT-1-CP-treated groups and the prolongation of QT intervals increased gradually along with the time of exposure to CT-1-CP. The QRS complex had no significant change in control group, one-week and three-week CT-1-CP-treated groups, but prolonged significantly in two-week and four-week CT-1-CP-treated groups. Interestingly, the QTd after chest-opening was significantly greater than that before chest-opening in control group(t=5.242, P<0.01), but decreased along with the time in CT-1-CP-treated groups. The mean MAP amplitude, Vmax and APD were greater in CT-1-CP-treated groups than those in control group, and became more obvious along with the time. The APD in four CT-1-CP-treat groups was prolonged mainly in middle to final repolarization phase. The difference among these groups became significant in middle phase(APD50)(F=6.076, P<0.01) and increased furthermore in late and final phases(APD70: F=10.054; APD90: F=18.691, P<0.01) along with the time of injection of CT-1-CP. The chronic action of CT-1-CP might induce the adapting alteration in cardiac conductivity and ventricular repolarization. The amplitude and the Vmax of the anterior LV epicardial MAP increased obviously, and the APD prolonged mainly in late and final phase of repolarization.