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1. 广东药学院基础学院
2. 中山大学中西医结合研究所
纸质出版日期:2012
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[1]刘颖,纪超,吴伟康.金属硫蛋白介导附子多糖对缺氧复氧心肌细胞的保护[J].中国实验方剂学杂志,2012,18(04):172-175.
LIU Ying1, JI Chao1, WU Wei-kang2. Metallothionein Mediates Protection by Fuzi Polymccharide on Neonatal Rat Cardiomyocytes with Hypoxia-reoxygenation[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(4): 172-175.
[1]刘颖,纪超,吴伟康.金属硫蛋白介导附子多糖对缺氧复氧心肌细胞的保护[J].中国实验方剂学杂志,2012,18(04):172-175. DOI: 10.13422/j.cnki.syfjx.2012.04.056.
LIU Ying1, JI Chao1, WU Wei-kang2. Metallothionein Mediates Protection by Fuzi Polymccharide on Neonatal Rat Cardiomyocytes with Hypoxia-reoxygenation[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(4): 172-175. DOI: 10.13422/j.cnki.syfjx.2012.04.056.
目的:以金属硫蛋白为着眼点
探讨附子多糖对缺氧复氧后心肌细胞的保护机制。方法:建立乳鼠心肌细胞缺氧/复氧模型
将乳鼠心肌细胞分为正常对照组、缺氧/复氧组、附子多糖组。缺氧/复氧组给予心肌细胞缺氧3 h后复氧6 h;附子多糖组分别给予10.0
1.0
0.1 g.L-1的附子多糖预处理心肌细胞24 h后再予缺氧3 h后复氧6 h。ELISA检测金属硫蛋白的含量
流式细胞仪检测细胞的凋亡率
测定心肌细胞内丙二醛(MDA)的含量和细胞培养液中乳酸脱氢酶(LDH)的含量。结果:与缺氧/复氧组相比较
附子多糖可以呈剂量依赖形式地增加金属硫蛋白的合成
减少MDA的生成与LDH的的释放
抑制心肌细胞凋亡
在10.0 g.L-1时作用达到峰值。结论:附子多糖对于缺氧复氧心肌细胞损伤具有保护效应
其机制与附子多糖促进金属硫蛋白的合成
对抗氧化应激损伤
抑制心肌细胞凋亡有关。
Objective:The present study was designed to use cultured neonatal rat cardiomyocytes with hypoxia-reoxygenation(H/R) to mimic in vivo ischemia-reperfusion injury(I/R)
and investigate the protective mechanism of fuzi polymccharide in cardiomyocytes against hypoxia-reoxygenation injury through metallothionein.Method:Cultured rat myocardial cells were divided into four groups:control
H/R
and fuzi polymccharide treatment groups.The cells in H/R group were incubated primarily in hypoxic buffer solution for 3 hours
thereafter
these cells were incubated for 6 hours in normal culture medium.The cells in fuzi polymccharide treatment group were cultured in medium added with 10.0
1.0
0.1 g·L-1 fuzi polymccharide for 24 hours before H/R.metallothionein of cardiomyocytes was measured by ELIZA
cell apoptosis of cardiomyocytes was measured by flow cytometry
MDA of cardiomyocytes and LDH in cell culture media were also measured.Result:As compared with H/R group
pretreatment with high and moderate dose of fuzi polymccharide increased the synthesis of metallothionein
decreased the synthesis of MDA and release of LDH.High dose of fuzi polymccharide decreased cardiomyocyte apoptosis.Conclusion:These data suggest that fuzi polymccharide pretreatment can protect cardiomyocytes from H/R injury.The mechanism is related to its enhancement of metallothionein synthesis
scavenging of oxygen free radical
and thus protection against apoptosis.
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