Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

二氮嗪减轻兔心肌缺血再灌注损伤后的心肌细胞凋亡

目的探讨二氮嗪对兔心脏缺血再灌注损伤过程中心肌细胞凋亡和心肌细胞bcl-2和bax基因表达的影响.方法24只兔随机分成假手术组(P组)、缺血再灌注组(IR组)、缺血预适应组(IP组)和二氮嗪组(DP组).阻断和松开左冠脉前降支制作缺血再灌注模型,缺血5 min/再灌注5 min连续3次循环诱导预适应.DP组在缺血前缓慢静脉注射二氮嗪3 mg/kg.再灌注结束后测算左室心肌梗死面积,取缺血区心肌行TUNEL法检测心肌凋亡细胞和免疫组化检测bcl-2和bax蛋白的表达.结果DP组和IP组梗死面积明显小于IR组(P＜0.001).凋亡细胞百分数DP组(34±5)%和IP组(32±6)%较IR组(56±8)%显著减少(P＜0.001).和IR组相比,bcl-2表达在IP组和DP组明显升高(P均＜0.01),bax基因表达在IP组和DP组则明显降低(P均＜0.001).结论二氮嗪能通过调节bcl-2和bax的表达来减轻兔心肌缺血再灌注损伤后的心肌细胞凋亡.     

EPO通过抑制心肌细胞凋亡保护糖尿病心肌病大鼠的心功能

目的探讨促红细胞生成素(erythropoietin,EPO)对糖尿病心肌病(diabetes cardiomyopathy,DCM)大鼠心脏的保护作用及机制。方法将25只SD大鼠随机分为3组:对照组(n=5)、DCM组(n=10)、DCM+EPO组(n=10),DCM组及DCM+EPO组应用链脲佐菌素60 mg/kg一次性腹腔注射构建DCM大鼠模型,饲养4周后,DCM+EPO组另外给予rhEPO 2 000 U/kg腹腔注射。行心脏超声心动图检测心功能,心肌HE染色、电镜检查,TUNEL染色测定细胞凋亡,Western Blot检测Caspase-3的表达,RT-PCR检测Bcl-2及Bax的mRNA的相对表达量。结果与对照组比较,DCM组和DCM+EPO组心功能降低(P<0.01),rh EPO能改善DCM+EPO组的心功能(P<0.01)。与对照组比较,DCM组及DCM+EPO组心肌细胞凋亡指数明显增加(P<0.001),rh EPO能改善DCM+EPO组的心肌细胞凋亡(P<0.001)。DCM组大鼠心肌的Caspase-3的蛋白表达量较正常组增加(P&l... 更多     

文山地区开展社区心脏康复的必要性及现状

随着社会经济的发展,人类生活方式的改变,心血管疾病发病率及死亡率是逐渐上升的,为降低其发病率及死亡率,必须采取预防防治手段,研究表明,心脏康复可以使心血管疾病患者从中获益,而心脏康复是一个长期持续性综合的过程,所以,开展社区心脏康复是一个发展趋势。本文主要从国内外开展社区心脏康复的现状、开展社区心脏康复的优点及必然趋势等方面进行研究,旨在总结出在文山地区开展社区心脏康复存在的问题及解决办法。     

昆明四区高血压病患者子代亲属流行病学调查

目的 了解昆明四区高血压患者子女高血压发病情况,分析高血压的影响因素.方法 对昆明四区>65岁者家庭行高血压调查,设1306例高血压病患者的子女为子代组,879例非高血压患者家庭的子女为对照组,分别记录性别、年龄、高血压发病情况及发病年龄.并调查高血压知晓率、治疗率及控制率情况.结果 与对照组比较子代组患病率、男性高血压、超重和腰围大于正常所占百分比高于对照组(P<0.05);子代组吸烟、饮酒比例高于对照组(P<0.05);子代组高血压知晓率、治疗率高于对照组(P<0.05).Logistic回归分析结果 提示超重、腰围大于正常、吸烟、饮酒和高盐饮食增加,患高血压的危险也随之增加(P<0.05).结论 子代高血压发病与生活方式(超重、腹型肥胖、吸烟、饮酒、高盐饮食)有关.     

体外培养猪骨髓间充质干细胞hHCN2基因的转染及表达

背景：通过超极化活化的阳离子电流调制心脏自律性成为该领域研究的焦点。目的：将起搏基因质粒CMV-hHCN2-3xha-IRES-EGFP转染到猪骨髓间充质干细胞,检测其在骨髓间充质干细胞中核酸和蛋白水平是否表达。方法：采用单纯直接贴壁法或密度梯度离心结合直接贴壁法分离、纯化、增殖获得骨髓间充质干细胞,脂质体2000转染质粒CMV-hHCN2-3xha-IRES-EGFP至骨髓间充质干细胞。结果与结论：单纯直接贴壁法收集到的细胞增殖速度慢,而密度梯度离心结合直接贴壁法细胞增殖速度较快,原代细胞培养第3代后转染48h荧光显微镜下可见骨髓间充质干细胞发出荧光,对照组无荧光。细胞转染率达15%-20%。RT-PCR检测及Westernblot印迹检测证明了hHCN2基因在骨髓间充质干细胞有表达。密度梯度离心结合直接贴壁法较单纯直接贴壁法培养骨髓间充质干细胞的培养效率更高。转染目的基因hHCN2的骨髓间充质干细胞蛋白有表达。     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

急诊经桡动脉冠脉介入治疗急性冠脉综合征中应用替罗非班的有效性和安全性

目的评估盐酸替罗非班对急性冠脉综合征(ACS)患者急诊经皮冠状动脉介入治疗(PCI)时防治无复流现象的作用以及安全性。方法 116例ACS患者随机分为盐酸替罗非班组和对照组,观察两组PCI术后TIMI血流级别、24 h肌钙蛋白T(CTnT)水平、24 h及30 d复合心血管终点事件发生率及出血情况。结果替罗非班组和对照组PCI术后TIMI 3级血流发生率分别为96.8%和88.9%,TIMI 0～2级血流发生率分别为3.2%和11.1%,P均<0.05。替罗非班组24 h CTnT水平较对照组降低(P<0.05),主要复合终点心血管事件发生率较对照组降低(P<0.05)。两组均无严重出血事件发生。结论盐酸替罗非班能明显降低ACS患者PCI术后无复流现象的发生,并改善无复流现象程度。