|
过氧化氢诱导心肌细胞凋亡性和非凋亡性死亡的研究 |
| |
曹纯章 杨绍娟 卜丽莎 杨同书
［摘 要］ 目的：探讨活性氧过氧化氢(H２O２)对心肌细胞损伤作用。方法：用不同浓度的H２O２作用于新生鼠培养心肌细胞，通过琼脂糖凝胶电泳、Giemsa染色和流式细胞仪等方法观察H２O２对心肌细胞的凋亡性损伤作用，同时检测培养介质中乳酸脱氢酶(LDH)和丙二醛(MDA)等生化指标的改变。结果：5 mmol/L H2O2作用于培养心肌细胞6 h，在琼脂糖凝胶电泳上出现梯状DNA带；Giemsa染色细胞涂片可见到染色体浓聚或边缘化，成新月型聚集在核膜周边，并有凋亡小体的存在；流式细胞仪可检测出亚二倍体峰的出现。结论：H２O２具有浓度和时间依赖关系诱导心肌细胞的凋亡，在低浓度H２O２(＜1 mmol/L)导致培养心肌细胞的早期生物化学改变，自由基含量升高，膜通透性增加，同时伴有少量心肌细胞凋亡；而在高浓度H２O２(＞10 mmol/L)时会造成培养心肌细胞的坏死性死亡，细胞膜崩塌，脂质过氧化物(MDA)大量产生，LDH大量泄漏，DNA琼脂糖凝胶电泳出现弥散(smear)泳带；5～10 mmol/L H２O２诱导大量心肌细胞凋亡性死亡，同时伴有LDH和MDA含量升高等生物化学的改变。
［主题词］ 氧；过氧化氢；心肌；细胞，培养的；细胞死亡
［中图分类号］ R363.21 ［文献标识码］ A
［文章编号］ 1000-4718(2000)05-0457-05
Study on apoptotic and nonapoptotic injuries induced by hydrogen peroxide in cardiac myocytes
CAO Chun-zhang, YANG Shao-juan, BU Li-sha, YANG Tong-shu
(Central Laboratory, Third Clinical Teaching College, Norman Bethune University
of Medical Sciences, Changchun 130031, China)
［Abstract］ AIM: To study apoptotic injury induced by reactive oxygen species-hydrogen peroxide (H２O２) on cardiac myocytes.METHODS:Cultured rat neonatal cardiac myocytes were treated with H２O２ of various concentration to observe apoptotic injury of cardiomyocytes by agarose gel electrophoresis, Giemsa-stained smears of cell, and flow cytometry, meanwhile lactate dehydrogenas (LDH) and malondialdehyde(MDA) were determined to assess the effect of H２O２ on lipid peroxidation and permeability of the plasma membrane. RESULTS: 5 mmol/L H２O2 caused cultured cardiomyocytes apoptotic morphological characteristics, including nucleosomal DNA fragmentation in myocytes by agarose gel electrophoresis (DNA ladder), cell shrinkage, nuclear condensation, and chromatin margin by Giemsa-stained cell smears, and aneuploid peak(AP)-apoptotic bodies occurrence by flow cytometry.CONCLUSIONS: H２O２-induced apoptosis in myocytes was a time-and concentration-dependent process. Treatment with low concentration of H２O２(＜1 mmol/L) o[1] [2] 下一页
上一个医学论文： 端粒酶活性与慢性粒细胞白血病病程关系的研究
下一个医学论文： 左旋多巴诱导PC12细胞凋亡及谷胱甘肽对细胞的保护作用
|
|
|
|
|
|
|
您现在的位置： 绿色健康网 >> 医学论文 >> 基础医学论文 >> 正文