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The effects of cyclosporine A (CsA) on Angiontensin Ⅱ (Ang Ⅱ )-induced protein contents, c-fos protein levels and cytosolic Ca2+ level ([Ca2+ ]i) in cultured cardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. [Ca2+ ]i labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confocal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang Ⅱ (10-7 mol/L), which could be inhibited by CsA in a dose-dependent manner. It was found that Ang Ⅱ could increase the c-fos protein expression, which could be inhibited by CsA in a dose-dependent manner.Ang Ⅱ induced the [Ca2+ ]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca2+ , but inhibited significantly the Ang Ⅱ-induced [Ca2+ ]i elevation. It was concluded that CsA can suppress the Ang Ⅱ-induced c-fos protein expression and [Ca2+ ]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang Ⅱ -induced cardiomyocyte hypertrophy by CsA.  相似文献
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Summary The effects of cyclosporine A (CsA) on Angiontensin II (Ang II)-induced protein contents, c-fos protein levels and cytosolic Ca2+ level ([Ca2+]i) in cultured cardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. [Ca2+]i labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confocal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang II (10−7 mol/ L), which could be inhibited by CsA in a dose-dependent manner. It was found that Ang II could increase the c-fos protein expression, which could be inhibited by CsA in a dose-dependent manner. Ang II induced the [Ca2+]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca2+, but inhibited significantly the Ang II-induced [Ca2+]i elevation. It was concluded that CsA can suppress the Ang II-induced c-fos protein expression and [Ca2+]i elevation in single cardiomyocyte, which might pay a role in the prevention of Ang II-induced cardiomyocyte hypertrophy by CsA. Han Zhaomin, female, born in 1974, Pharmacist  相似文献
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目的 利用细胞实验探讨高糖培养对H9C2细胞凋亡的影响,并探讨苯磺酸氨氯地平的保护作用.方法 体外培养大鼠心肌细胞H9C2,分为5 mmol/L糖培养组(G1)、25 mmol/L糖培养组(G2)、50 mmol/L糖培养组(G3)和25 mmol/L糖培养组加钙离子通道抑制剂络活喜保护组(G2+N)、50 mmol/L糖培养组加络活喜保护组(G3+N)5组,每组分设48 h(a)、72 h(b)培养两个亚组共10组.AnnexinV/PI结合流式细胞仪检测细胞凋亡率,荧光染色观察[Ca2十]i.结果 细胞凋亡率随着高糖刺激时间和高糖浓度的增加而逐渐增高,加络活喜组细胞的凋亡率显著降低(P<0.05).G2、G3组单细胞平均[Ca2+]i活性测定荧光值均较G1组升高(P<0.05);G2+N、G3+N组单细胞平均[Ca2+]i活性测定荧光值分别较G2、G3组降低(P<0.05).各a、b亚组间单细胞平均[Ca2+]i活性测定荧光值差异无统计学意义(P>0.05).结论 高糖培养H9C2细胞可增加[Ca2+]i从而导致细胞凋亡,苯磺酸氨氯地平可抑制Ca2内流从而抑制细胞凋亡.  相似文献
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目的 探讨AKT通路在血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥大中的作用,及硫氧环蛋白过氧化物酶3(Peroxiredoxin-3,Prdx-3)对此作用的影响.方法 体外培养心肌细胞(H9C2)随机分为对照组、AngⅡ组(10-7mol/L)、AngⅡ+转染对照组和AngⅡ+Prdx-3转染组.脂质体转染法将Prdx-3表达质粒转染心肌细胞,western blot法检测Prdx-3及磷酸化AKT (p-AKT)蛋白表达,Real-time PCR法检测脑钠素(BNP) mRNA表达,二氯荧光素二乙酸(DCFH-DA)检测活性氧(ROS)水平.结果 Prdx-3表达质粒转染心肌细胞后,Prdx-3蛋白表达值为0.94±0.10,高于转染对照组(0.35±0.04),差异有统计学意义(P<0.01).与对照组比较,AngⅡ组BNP mRNA[(1.0±0.0)比(1.63±0.24)]、ROS水平[(3 631±317)比(4 678±270)]及p-AKT蛋白表达[(0.13±0.05)比(0.44±0.09)]均明显增加,差异有统计学意义(P<0.01).AngⅡ+转染对照组和AngⅡ组的BNP mRNA[(1.77±0.22)比(1.63±0.24)]、ROS[(4 401±308)比(4 678±270)]及p-AKT蛋白水平[(0.53±0.08)比(0.44±0.09)]差异无统计学意义(P>0.05).与AngⅡ组比较,AngⅡ+Prdx-3转染组BNP mRNA[(1.63±0.24)比(1.28±0.18)]、ROS [(4 678±270)比(3 933±237)]及p-AKT蛋白水平[(0.44±0.09)比(0.20±0.05)]明显下降,差异有统计学意义(P<0.05).结论 AngⅡ通过线粒体来源的ROS激活AKT通路,诱导心肌细胞肥大,而高表达Prdx-3可通过降低ROS水平来抑制AngⅡ的作用.  相似文献
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目的:观察硫氧环蛋白过氧化物酶3(Prdx-3)在血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥大中的作用,并探讨其作用机制。方法体外培养心肌细胞(H9C2)随机分为对照组、AngⅡ组、AngⅡ+转染对照组和AngⅡ+Prdx-3转染组。脂质体转染法将Prdx-3表达质粒转染心肌细胞,Western blot法检测Prdx-3蛋白表达,Real-time PCR法检测脑钠素(BNP)mRNA表达,二氯荧光素二乙酸(DCFH-DA)检测活性氧(ROS)水平。结果 Prdx-3表达质粒转染心肌细胞后,Prdx-3蛋白表达值为(0.88±0.12),高于转染对照组(0.38±0.05),差异有统计学意义(P<0.05)。与对照组比较,AngⅡ组BNP mRNA[(1.00±0.00)比(1.72±0.29)]、ROS[(3473±81)比(4439±111)]及Prdx-3蛋白表达水平[(0.33±0.05)比(0.72±0.14)]均明显增加,差异均有统计学意义(均P<0.05)。 AngⅡ+转染对照组和AngⅡ组的BNP mRNA [(1.72±0.29)比(1.94±0.34)]、ROS [(4439±111)比(4285±167)]及Prdx-3蛋白水平[(0.72±0.14)比(0.75±0.11)]比较,差异无统计学意义(P>0.05)。与AngⅡ组比较,AngⅡ+Prdx-3转染组BNP mRNA [(1.72±0.29)比(1.29±0.15)]和ROS水平[(4439±111)比(3648±254)]明显下降,但Prdx-3蛋白水平[(0.72±0.14)比(1.89±0.37)]显著增高,差异均有统计学意义(均P<0.05)。结论 AngⅡ可通过ROS诱导心肌细胞肥大,而Prdx-3通过降低ROS抑制AngⅡ的作用。  相似文献
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机械负荷过度将导致病理性心肌肥大并严重危害人类健康。机械刺激作用于心肌细胞后,可通过细胞表面的机械感受器(如整合素)或分泌细胞因子(血管紧张素Ⅱ及内皮素等),激活一系列信号通路,主要的有丝裂原激活蛋白激酶通路、詹纳斯激酶/信号转导蛋白转录激活因子通路及由钙离子介导的信号通路。心肌细胞将机械信号转化为化学信号,调节肥大相关基因的表达,致使心肌细胞发生肥大。  相似文献
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赵文菊  李刚  李俊 《医学综述》2012,(20):3353-3355
环腺苷酸结合蛋白(Epac)是环磷酸腺苷激活作用于Ras样GTP酶的鸟嘌呤核苷酸交换因子。现已确认Epac参与调控包括Ca2+离子处理,细胞增殖,细胞生存,细胞生化,细胞极化,细胞-细胞黏附事件等关键的细胞过程。最近研究表明,Epac在调控炎症和心肌肥厚中发挥着重要作用。现就Epac信号途径及其与心肌细胞肥大的关系进行综述,以便进一步了解Epac在心脏功能中的作用。  相似文献
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李劲松 《重庆医学》2011,40(25):2537-2538,2540
目的探讨环氧化酶-2(COX-2)在高糖高胰岛素诱导的心肌肥大中的作用。方法用高糖高胰岛素刺激体外培养的乳鼠心肌细胞,以细胞表面积、蛋白含量和心房利钠因子(ANF)mRNA表达为心肌细胞肥大的反映指标,观察COX-2特异性抑制剂———赛来昔布对高糖高胰岛素致肥大作用的影响。利用real-time PCR检测细胞中mRNA的表达。结果高糖高胰岛素诱导细胞表面积、总蛋白含量以及ANF、COX-2 mRNA的表达增加(P<0.05);赛来昔布可以抑制高糖高胰岛素诱导的心肌细胞肥大(P<0.05),同时抑制COX-2的表达(P<0.05)。结论赛来昔布可以通过抑制COX-2的表达,从而对抗高糖高胰岛素诱导的心肌肥大。  相似文献
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目的:探讨甲状腺素致心肌细胞肥大的相关机制。方法:取分离培养的乳鼠心肌细胞,用L-甲状腺素(T3)诱导心肌细胞肥大,然后再加入磷脂酰肌醇-3-激酶(PI3-K)抑制剂LY294002和哺乳动物雷帕霉素靶蛋白(mTOR)特异性抑制剂雷帕霉素进行干预;采用测量心肌细胞表面积及3H-亮氨酸掺入、Western blot等检测方法。结果:甲状腺素诱导的心肌细胞肥大能被LY294002或雷帕霉素抑制,LY294002能抑制甲状腺素激活丝氨酸/苏氨酸激酶(AKT)和mTOR,雷帕霉素能特异性阻断mTOR的活化。结论:甲状腺素能通过PI3-K/Akt-mTOR信号通路促进心肌细胞肥大。  相似文献
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