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High glucose induces myocardial cell injury through increasing reactive oxygen species production

Asian Pacific Journal of Tropical Medicine 2018年第1期11卷 63-67页

作者： Yu-Jun Wang Xiao-Yu Lyu Li Yu Department of Critical Care Medicine the Central Hospital of WuhanTongji Medical CollegeHuazhong University of Science and Technology Department of Endocrinology the Central Hospital of WuhanTongji Medical CollegeHuazhong University of Science and Technology

Objective: To study the injury effect and molecular mechanism of high glucose on myocardial cells. Methods: myocardial cells H9 c2 were cultured and divided into the control group treated with DMEM containing 5.5 mmol/L glucose, the high glucose group treated with DMEM containing 35 mmol/L glucose, and the N-acetylcysteine(NAC) group pre-treated with 1000μmol/L NAC and treated with DMEM containing 1000 μmol/L NAC and 35 mmol/L *** production of ROS and the expression of mitochondria pathway apoptosis molecules in cells as well as the contents of collagen and collagen metabolism molecules were ***: After 8 h, 16 h and 24 h of treatment, ROS RFU as well as Bax, CytC, Caspase-3 and Caspase-9 protein expression in cells and Col-I, Col-Ⅲ, PINP and PⅢNP protein levels in culture medium of high glucose group were higher than those of control group, Bcl-2 protein expression were lower than those of control group, but CTX-Ⅰ protein levels in culture medium were not significantly different from those of control group; after 24 h of treatment, Bax, CytC,Caspase-3 and Caspase-9 protein expression in cells as well as Col-Ⅰ, Col-Ⅲ, PINP and PIIINP protein levels in culture medium of NAC group were lower than those of high glucose group whereas Bcl-2 protein expression was higher than that of high glucose group. Conclusions:High glucose can induce myocardial cell apoptosis, increase collagen synthesis and accelerate interstitial fibrosis by increasing the production of reactive oxygen species.

关键词： Diabetic cardiomyopathy High glucose myocardial cells Reactive oxygen species Apoptosis Collagen

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Investigation of the Distribution and Changes of VLDLR Subtype in Fibrotic Cardiac Muscles

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2000年第4期20卷 297-300页

作者：杨光田鲍力赵金平屈伸 Department of Emergency Tongji Hospital Tongji Medical University Wuhan Department of Biochemistry Tongji Medical University Wuhan Department of Cardiothoracic Surgery Tongji Hospital Tongji Medical University Wuhan

Very low-density lipoprotein receptor (VLDLR) is the major receptor with which cells can uptake the triacylglycerol from blood. It is divided into two subtypes according to presence of O- linked sugar domain located in the VLDLR receptor immediately outside of the membrane. Type Ⅰ VLDLR contains the O-link domain, while type Ⅱhas no such domain. The type ⅠVLDLR are mainly found on the surface of human myocardial cells. The result of our quantitative polymerase chain reaction on the normal and fibrotic cardiac muscles showed that both subtypes and expression level of VLDLR on the myocardial cell surface did not vary significantly between the normal and the fibrotic cardiac muscles despite the presence of malfunction due to fibrosis. This finding suggests that fibrosis doesn't exert significant influence on the subtype and the expression of VLDLR on the sur- face of myocardial cells. Such inconsistence with the changes found in other fibrotic tissues is awaiting further studies.

关键词： myocardial cells cardiac muscle fibrosis very low-density lipoprotein receptor (VLDLR)

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Protective Effect of Thrombopoietin on myocardial Cell in Vitro

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South China Journal of Cardiology 2008年第4期9卷 193-198页

作者：黄伟哲肖大伟郑育举欧晓敏谢泽锋 Department of Cardiothoracic Surgery The First Affiliated Hospital of Shantou University

Objectives To investigate the protective effect of thrombopoietin (TPO) on myocardial cells in vitro. Methods H9C2 cell line was maintained in Iscove’s modified Dulbecco’s medium (IMDM) supplemented with 10% calf serum. Beating cells from heart ventricles of neonatal heart were cultured at an in vitro system. Apoptosis of the cell line above was induced by treatment of doxorubicin (DOX) and was blocked by TPO. Cell survival rate of H9C2 cell was measured by the MTT assay. Changes of beating rate of neonatal myocardial cells were captured by digital camera and beating rate was calculated. Flow cytometry was employed to study anti-apoptotic effect of TPO by staining JC-1 protein to H9C2 cell. Results MTT assay demonstrated that doxorubicin reduced cell survival rate by 73.8%±1.1%, 50 ng·mL-1 and 100 ng·mL-1 TPO increased cell survival rate by 84.6%±3.6% (Pmyocardial cells also decreased to 15%±8% at 48 h, 100 ng·mL-1 TPO improved beating rate to 48%±11% (Pmyocardial cells in vitro. Anti-apoptosis is one of the mechanisms by which TPO protects injured heart.

关键词： thrombopoietin doxorubicin myocardial cells apoptosis

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Role of cytoskeleton in the mechanisms of stretch-induced cardiomyocytical hypertrophy in vitro

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Journal of Medical Colleges of PLA(China) 2001年第1期16卷 1-3页

作者：冯兵覃军何作云王德文 Department of Cardiology Xinqiao Hospital Third Military Medical University Chongqing 400037 China

Objective: To study in vitro the role of cytoskeleton in the mechanisms of stretch-induced cardiomyocyte hypertrophy. Methods: After cultured on a deformable membrane, the myocardial cells were incorporated with 3H-leucine (3H-leu) to determine the hypertrophic rate. The contents of angiotensin II and endothelin in the supernatant of the culture medium were measured with radioimmunoassay. Results: Colchicine at 4 μmol/L partially inhibited 3H-leu incorporation rate of the stretch-induced cardiomyocytes but cytochalasin B showed no such effect. The radioactivity of 3H-leu incorporation in the supernatant of the culture medium was significantly lower in the cardiomyocyte culture treated with colchicines (μmol/L) or cytochalasin (0.4μmol/L) than in simple myocardial cell culture. In addition, the 2 agents markedly inhibited the myocardial cells from secreting angiotensin II and endothin. Conclusion: The cytoskeleton plays a role in the stretch-induced mycardiocyte hypertrophy by mediating the secretion of the cell growth factors by the cells themselves.

关键词： cytoskeleton stretching myocardial cells hypertrophy autocrine

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晚期恶性肿瘤患者阿霉素疗程前后心肌的亚微结构改变

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西安交通大学学报(医学版) 1986年第3期 235-237页

作者：陈金典杨少毅西安医科大学电子显微镜室西安医科大学电子显微镜室

阿霉素(ADR)可致卉叶量依赖性心肌病,故临床化疗往往受到限制。为了解其对心肌的毒性作用,我们对5例晚期恶性肿瘤患者(骨肉瘤2例;纤维肉瘤、肝癌、恶性淋巴瘤各1例),分别在阿霉素化疗前后,各取心内膜心肌活检进行电镜观察,并对比其亚细... 详细信息

阿霉素(ADR)可致卉叶量依赖性心肌病,故临床化疗往往受到限制。为了解其对心肌的毒性作用,我们对5例晚期恶性肿瘤患者(骨肉瘤2例;纤维肉瘤、肝癌、恶性淋巴瘤各1例),分别在阿霉素化疗前后,各取心内膜心肌活检进行电镜观察,并对比其亚细胞结构之改变。结果发现:化疗前少数细胞质膜局部缺损,肌质网、横管呈囊泡状扩张,闰盘间隙扩大;线粒体增生,部分肿胀退变,心肌原纤维局灶性溶解脱失。胞质内脂褐素颗粒增多。化疗后以上病变继续存在且加重,并见部分线粒体内外膜溶解消失,仅呈嵴群堆集残留者。胞质内出现小脂滴,脂褐素颗粒更为增多。

关键词： adriamycin malignant tumors ultrastructural cnanges myocardial cells

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