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蛋白激酶C(PKC)与心衰 被引量:4
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作者 陈文政 柏树令 《解剖科学进展》 CAS 2001年第2期140-142,共3页
心衰是一种严重威胁人类健康和生活质量的疾病。研究表明 ,PKC存在于心脏所有的细胞内 ,当发生心衰时 ,不同亚型的PKC表达提高 ,通过进一步研究发现PKC在心衰细胞中作为肥大信号传导 ,从而推进了心衰功能障碍机理的研究 ,开辟出治疗心... 心衰是一种严重威胁人类健康和生活质量的疾病。研究表明 ,PKC存在于心脏所有的细胞内 ,当发生心衰时 ,不同亚型的PKC表达提高 ,通过进一步研究发现PKC在心衰细胞中作为肥大信号传导 ,从而推进了心衰功能障碍机理的研究 ,开辟出治疗心衰的一条新路 。 展开更多
关键词 蛋白激酶C PKC 结构特点 检测 心衰肌细胞
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Review:Cell therapy in congestive heart failure 被引量:4
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作者 TAO Ze-wei LI Long-gui 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2007年第9期647-660,共14页
Congestive heart failure (CHF) has emerged as a major worldwide epidemic and its main causes seem to be the aging of the population and the survival of patients with post-myocardial infarction. Cardiomyocyte dropout... Congestive heart failure (CHF) has emerged as a major worldwide epidemic and its main causes seem to be the aging of the population and the survival of patients with post-myocardial infarction. Cardiomyocyte dropout (necrosis and apoptosis) plays a critical role in the progress of CHF; thus treatment of CHF by exogenous cell implantation will be a promising medical approach. In the acute phase of cardiac damage cardiac stem cells (CSCs) within the heart divide symmetrically and/or asymmetrically in response to the change of heart homeostasis, and at the same time homing of bone marrow stem cells (BMCs) to injured area is thought to occur, which not only reconstitutes CSC population to normal levels but also repairs the heart by differentiation into cardiac tissue. So far, basic studies by using potential sources such as BMCs and CSCs to treat animat CHF have shown improved ventricular remodelling and heart function. Recently, however, a few of randomized, double-blind, placebo-controlled clinical trials demonstrated mixed results in heart failure with BMC therapy during acute myocardial infarction. 展开更多
关键词 Congestive heart failure Acute myocardial infarction Myocardial regeneration Cell therapy
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Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats
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作者 李为民 刘巍 +2 位作者 孙宁玲 陈源源 虞有智 《Chinese Medical Journal》 SCIE CAS CSCD 2002年第3期364-366,共3页
OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs)... OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P 展开更多
关键词 Animals Antihypertensive Agents Apoptosis CARDIOMEGALY Hypertension Myocardium RATS Rats Inbred SHR Rats Wistar TETRAZOLES VALINE
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