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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】体外培养新生大鼠心肌细胞,观察AngⅡ在诱导细胞肥厚过程中对Kv4.2蛋白表达的影响,及钙离子在其细胞内信号传导通路中的作用。【方法】AngⅡ心肌细胞肥大模型,用激光共聚焦显微镜检测AngⅡ对心肌细胞胞浆钙离子浓度的影响,用流式细胞仪检测AngⅡ诱导心肌细胞肥厚过程中细胞Kv4.2表达的变化。【结果】AngⅡ明显增加细胞的蛋白总量,诱导心肌细胞肥大,AngⅡ能增加心肌细胞胞浆钙离字浓度,下调Kv4.2编码的通道蛋白的表达含量。【结论】AngⅡ在诱导心肌细胞肥大过程中,可能通过细胞内钙离子以外的信号通路下调Ito通道蛋白Kv4.2。  相似文献   

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耿鹏  吴扬  杨惠超  刘娟 《南通医学院学报》2010,23(1):24-27,F0002
目的:探讨辛伐他汀对心肌细胞肥大的防治作用及其与钙通道活动的关系。方法:采用血管紧张素Ⅱ诱导新生大鼠心肌细胞肥大模型。应用改良Lowry法测定心肌细胞总蛋白含量。相差显微镜测定心肌细胞表面积。CCK-8法检测心肌细胞活力变化。westernblot方法检测心肌细胞L-型钙通道亚单位Cav1.2(α1C)、T-型钙通道亚单位Cav3.1(α1G)、Cav3.2(α1H)蛋白表达的变化。应用激光共聚焦显微镜技术检测[Ca^2+]i的变化。结果:(1)辛伐他汀能明显抑制AngⅡ诱导的心肌细胞总蛋白含量及细胞表面积的增加,同时提高心肌细胞活力;(2)辛伐他汀能明显降低心肌细胞T-型钙通道α1G、α1H蛋白表达,但对L-型钙通道α1C蛋白表达无明显影响;(3)辛伐他汀可呈剂量依赖性抑制心肌细胞肥大所致的钙离子超载。结论:辛伐他汀对AngⅡ诱导的心肌细胞肥大具有明显的防治作用,其作用机制可能与辛伐他汀抑制T-型钙通道α1G、α1H蛋白的重新再表达有关,并与其抑制细胞内钙超载密切相关。  相似文献   

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[目的]在原代培养的大鼠乳鼠心肌细胞上,观察乌苏里藜芦生物碱(Veratrum nigrum L.Var.ussurience Na-kai alkaloids,VnA)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的大鼠乳鼠的心肌细胞肥大的影响。[方法]通过BCA法测定心肌细胞蛋白含量和显微测微器测定心肌细胞直径,免疫荧光法分析心肌细胞内钙调神经磷酸酶(calcineurin,CaN)的表达变化。[结果]在一定剂量范围内VnA能抑制心肌细胞蛋白含量的增加(P<0.01)和细胞体积的增加(P<0.01),细胞内CaN的表达减少。[结论]VnA抑制AngⅡ诱导的乳鼠心肌细胞肥大可能与其抑制细胞内CaN表达有关。  相似文献   

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目的研究mAKAPβ蛋白在AngⅡ促新生大鼠心肌细胞肥大中的作用及其机制。方法观察AngⅡ刺激下大鼠心室肌细胞形态学变化及细胞内mAKAPβ蛋白表达水平的变化。使用RNA干扰技术抑制mAKAPβ蛋白表达,观察在此条件下AngⅡ促新生大鼠心肌细胞肥大作用的变化,同时观察ERK2蛋白磷酸化水平的变化。结果在AngⅡ刺激下,大鼠心肌细胞面积明显增大,ANP表达水平明显升高,P-ERK水平明显升高,但mAKAPβ蛋白表达水平无明显改变。使用RNA干扰技术抑制mAKAPβ蛋白表达后,AngⅡ促新生大鼠心肌细胞肥大的表现明显减弱甚至消失。结论AngⅡ有明显的促新生大鼠心肌细胞肥大作用,mAKPβ蛋白在此过程中发挥着重要作用。  相似文献   

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孔宏亮  李占全  袁龙 《广东医学》2012,33(2):167-169
目的在血管紧张素Ⅱ(AngⅡ,CoCl2)诱导乳鼠心肌细胞肥大基础上,探讨人参皂苷Rb1(ginsen-oside Rb1,Gs-Rb1)是否可通过一氧化氮合酶/一氧化氮(NOS/NO)系统减轻心肌细胞肥大。方法将乳鼠心肌细胞随机分为对照组、AngⅡ组、Gs-Rb1组、Gs-Rb1+L-NAME(NOS抑制剂)组、Gs-Rb1+AngⅡ+L-NAME组,AngⅡ、L-NAME和Gs-Rb1浓度分别是10μmol/L、1 mmol/L和200μmol/L;分别测定心肌细胞表面积、细胞培养液NO浓度和心肌细胞NOS活性。结果 (1)Gs-Rb1显著抑制AngⅡ所致的心肌细胞肥大(P=0.00),但不能使心肌细胞回复到正常大小;Gs-Rb1减小心肌细胞表面积的效应可被L-NAME显著抑制(P=0.00)。(2)AngⅡ降低心肌细胞NO浓度的效应可被Gs-Rb1显著抑制(P=0.00),但L-NAME可完全抑制Gs-Rb1对心肌细胞的NO分泌效应。(3)Gs-Rb1显著增加心肌细胞在AngⅡ干预时的NOS活性(P=0.00),该效应被L-NAME完全抑制。(4)心肌细胞表面积与NOS(r=0.59,P=0.00)、NO(r=0.62,P=0.00)均呈正相关。结论 Gs-Rb1显著抑制AngⅡ所致的心肌细胞肥大,此效应至少部分通过NOS/NO系统实现。  相似文献   

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通过^3H-Leu掺入量的测定与RNA狭线杂交技术,初步探讨血管紧张素Ⅱ受体,Ca^2+在血管紧张素Ⅱ刺激乳鼠心肌细胞蛋白质合成中的作用,并观察血管紧张素Ⅱ对原癌基因c-fos表达,结果发现培养液中加入钙通道阻断剂(verapamil),细胞外钙螯合剂(EGTA),肌浆网钙释放抑制剂(dantrolene)和细胞内钙螯合剂(Fura-2/AM)可使血管紧张素Ⅱ介导的^3H-Leu掺入量较单独加血管  相似文献   

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Objective To explore the effect of atorvastatin on cardiac hypertrophy and to determine the potential mechanism involved. Methods Anin vitro cardiomyocyte hypertrophy from neonatal rats was induced with angiotensinⅡ (AngⅡ) stimulation. Before AngⅡ stimulation, the cultured rat cardiac myocytes were pretreated with atorvastatin at different concentrations (0.1, 1, and 10μmol/L). The following parameters were evaluated: the myocyte surface area,3H-leucine incorporation into myocytes, mRNA expressions of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase 9, matrix metalloproteinase 2, and interleukin-1β, mRNA and protein expressions of theδ/β peroxisome proliferator-activated receptor (PPAR) subtypes. Results It was shown that atorvastatin could ameliorate AngⅡ-induced neonatal cardiomyocyte hypertrophy in the area of cardiomyocytes,3H-leucine incorporation, and the expression of atrial natriuretic peptide and brain natriuretic peptide markedly. Meanwhile, atorvastatin also inhibited the augmented mRNA level of several cytokines in hypertrophic myocytes. Furthermore, the down-regulated expression of PPAR-δ/β at both the mRNA and protein levels in hypertrophic myocytes could be significantly reversed by atorvastatin treatment. Conclusions Atorvastatin could improve AngⅡ-induced cardiac hypertrophy and inhibit the expression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.  相似文献   

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