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This study is to observe the protection of gross saponins of Tribulus terrestris (GSTT) on cardiocytes impaired by adriamycin (ADR) and approach its mechanism of action. Cardiocytes of neonate rat were cultivated for 72 hours and divided into normal control group, model (ADR 2 mg?L-1) group, and GSTT (100, 30, and 10 mg?L-1) groups. MTT colorimetric method was deployed to detect cardiocyte survival rate, activities of CK, LDH, AST, SOD, MDA and NO were detected, and apoptosis was detected with flow cytometry. Effect of GSTT on caspase-3 was detected with Western blotting. Compared with control group, contents of CK, LDH, AST, MDA and NO were increased, and activity of SOD was reduced (P
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@#Objective To detect the strain features of regional wall abnormalities in patients with coronary artery disease during each diastolic period, and its possibility to evaluate regional left ventricular cardiocyte viability and diastolic function.Methods 54 patients with anterior myocardial infarction (MI group) and 78 normal subjects (NOR group) underwent Doppler tissue imaging, which were performed in 2-chamber-view by strain curves synchronously.Results In the NOR group, strain value of 66 cases (84.62%) showed an gradually increasing negative value from the apex to base to middle of left ventricle, while in the MI group, there were 9 cases (16.67%) with such a trend. IR phase: in the NOR group, 564 segments (90.38%) were upward wave bands, but in the MI group, there were 123 segments (28.47%) having such waves ( P<0.05). RF phase: in the NOR group, 576 segments (92.31%) were upward and steep wave bands, but in the MI group, the number of upward waves were obviously less (102 segments,23.61%) ( P<0.01). SF period: compared with the NOR group, which was horizontal, the MI group had upward wave bands ( P<0.05).Conclusion Regional myocardial ischemia and infarction can cause significant regional diastolic wall abnormalities of strain value in active diastolic phase. Regional diastolic wall motion abnormalities can be evaluated quantitatively and synchronously with high sensitivity by strain curve which has the potential value in cardiocyte viability and diastolic function.
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@# It was thought that cardiocyte necrosis is the only dead form after acute myocardial infarction. Recent researches have demonstrate that apoptosis and necrosis both are dead forms of cardiocyte, which play important role in the ventricular remodeling after acute myocardial infarction.
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Objective To investigate the effects and mechanisms of extract of ginkgo biloba(EGb)on the cell of cardiocyte hypertrophy induced by prostaglandin F2 alpha.Methods normal cells were used as negative control,and spontaneously PGF2? and EGb were used as experimental groups.The cells were isolated and cultured on cultured neonatal rat cardiocyte by PGF2?,cardiocyte hypertrophy was determined by the cell surface and the total protein of cells;the level of intracellular ROS measured by the fluorescence microscope.Results In cardiocyte hypertrophy,the cell surface,the level of intracellular ROS and the total protein of cells increased significantly in cutured neonatal rat cardiac treated with PGF2?.Compared with cells treated with PGF2?,EGb(40?g/ml,80?g/ml,100?g/ml)inhibited cardiocyte hypertrophy by PGF2?-induced,decreased in the cell surface by 19%,27%,33% and in the total protein of cells by 21%,39%,47% respectively(all P
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Objective:To expound the effect of Kangxianyixin prescription on cardiocyte apoptosis and expression of Bax and Bcl-2 in rats with dilated cardiomyopathy. Methods:Wistar rats with dilated cardiomyopathy established by furazolidone were treated 8 weeks with Kangxianyixin prescription,to observe cardiocyte apoptosis and to measure Bax and Bcl-2 expression in rats. Results:(1) In comparison of cardiomyocyte apoptosis indexes in rats,when compared with model group,the results showed significant difference in the combined group of high dosage of Kangxianyixin prescription and captopril,the high dosage group,the low dosage group,the captopril group(P
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3?10 -4 mol/L), and the role was persistent if its concentration was kept. Meanwhile, the increase of intracellular free Ca 2+ induced by stretch was also inhibited by NO. Conclusion Cardiocytes hypertrophic response stimulated by stretch could be inhibited by nitric oxide. The inhibitory effect might be due to the decrease of the concentration of intracellular free Ca 2+ .
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Objective To examine effects of hydrogen peroxide on intracellular free calcium concentration(i) in cardiac myocytes and its antagonism by carvedilol. Methods A cell culture of neonatal rat cardiac myocytes was used for experimentation. They were divided into four groups, i.e. control group, hydrogen peroxide (H 2O 2) group, carvedilol group,and H 2O 2 + carvedilol group. Confocal microscope was used with Fluo-3/AM as calcium indicator to detect changes in i immediately and 15 minutes after H 2O 2 intervention, respectively. Results The intracellular fluoresence intensity of a single cardiae myocyts in the control group and carvedilol group was low. The intracellular fluoresence intensity of a single cardiac myocyte in H 2O 2 group was significantly higher than in the control group 15 minutes after intervention (P
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10?m cytochalasin D (CD) was used to treat cardiocytes from adult human atrium and adult rat atrium and ventricle in long-term primary cultures. Durations of treatment were 0.5, 1, 6, 12, 24 and 48h. In some cultures, the medium containing CD was removed at the planned time to be replaced with the medium without CD.These dishes were then cultured for an additional 48h. Control cultures were exposed to dimethyl sulfoxide (DMSO), the vehicle used to dissolve CD. All cultured cells were first stained with rhodamine-labelled phalloidin to show F-actin and then stained with fluoreseein-labelled antitubulin to show microtubles. The freshly isolated and rounded cardiocytes did not respond to CD, while the spreading cells responded apparently. The actin filament bundles in the peripheral zone of spreading cells were cut into segments. Most segments were gathered into aggregates and granules. Some aggregates were lodged on the inner aspect of the sarcolemma. Small vacuoles were seen between the myofibrils or somewhere along the course of the myofibrils. The CD response from the atrial spreading cells, especially the human atrial spreading cells, were more obvious than that from the rat ventricular cells. Cells exposed to CD and then cultured in normal medium for 48h did not return to normal. Microtubules were not directly affected by CD, but in places where vacuolization occured they made way for vacuoles. All the control cultures made no response to DMSO. The above-mentioned results suggest that different sensitivity to CD existed in cultured adult cardiocytes between different species and that a difference also existed in the contractile machinery between the atrial culturing cells and ventricular cultureing cells of the same species.
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The relationship between the morphological development and the contents of glycogen, LDH, SDH in the beating as well as beat arrested cardiocytes cultured in vitro was studied cytochemically in neonatal rats. The results showed that. (1) After the cardiocytes were inoculated, they did not start to beat until they developed to elongated cells with some processes or stellated cells, and the contents of glycogen, LDH and SDH in cardiocytes reached to a given threshold (score) respectively. In beat arrested cells the contents of glycogen, LDH and SDH were below the beat-starting thresholds. (2) The greater the cell density of cardiocytes was, the more strongly the cell clusters beated. The cell density of cardiocytes was increased by mitosis. In 48-72h, cell divisions occurred in part of cardiocytes. Most mitotic figures were observed in 120h. When mitosis was in progress, cardiocytes containing glycogen particles became short but still with some branched processes. As the cardiocyte clusters were formed, the beat occurred strongly. The cytochemical reactions mentioned above may be used to evaluate how serious the cell is damaged in cytotoxicological and pharmalogical research.