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促红细胞生成素对心肌细胞氧化损伤的保护作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第2期
页码:
183-185
栏目:
基础研究
出版日期:
2010-03-04

文章信息/Info

Title:
Protective effect of erythropoietin on oxidative injury in cultured rat cardiomyocytes
作者:
宗刚军吴刚勇王霄夏阳张丽陈满清陈景开
解放军第101医院心内科,江苏 无锡 214044
Author(s):
ZONG Gang-jun WU Gang-yong WANG Xiao XIA Yang ZHANG Li CHEN Man-qing CHEN Jing-kai
Department of Cardiology, PLA 101 Hospital, Wuxi 210044, Jiangsu, China
关键词:
重组人促红细胞生成素心肌细胞氧化损伤钠钾泵
Keywords:
recombinant human erythropoietin cardiomyocytes oxidative injury Na+-K+-ATPase
分类号:
Q58
DOI:
-
文献标识码:
A
摘要:
目的: 探讨重组人促红细胞生成素(rhEPO)对体外培养的乳鼠心肌细胞氧化损伤的保护作用及其机制。方法: 建立低浓度过氧化氢诱导原代培养的乳鼠心肌细胞氧化损伤的模型后,用rhEPO进行干预,以噻唑蓝(MTT)比色法检测rhEPO对细胞存活的影响。同时通过检测培养介质中乳酸脱氢酶(LDH)活力、丙二醛(MDA)含量及心肌细胞内钠-钾ATP酶(Na+-K+-ATPase)、谷胱甘肽过氧化物酶(GSH-PX)活力的改变,评价EPO对心肌细胞的保护作用,并探讨其作用机制。结果: 在低浓度过氧化氢的作用下,体外培养的心肌细胞的存活率降低(P<0.05)。rhEPO可明显改善心肌细胞的存活率(P<0.05),使培养介质中LDH和MDA的水平显著下降(P<0.05),细胞内Na+-K+-ATPase和GSH-PX活力显著提高(P<0.01),同时细胞结构得到改善。结论: rhEPO可对抗过氧化氢致心肌细胞损伤,作用机制与其抑制脂质过氧化和提高细胞内钠钾泵活力的作用有关。
Abstract:
AIM: To explore the protective effect and mechanism of recombinant human erythropoietin (rhEPO) on cardiomyocytes against oxidative injury. METHODS: An experimental model of oxidative injury was established using cultured neonatal rat cardiomyocytes. The survival rate of cultured cardiomyocytes incubated in the presence or absence of rhEPO was examined using the MTT assay. Myocyte damages were estimated by release of lactate dehydrogenase (LDH) and cellular structure. Malondialdehyde (MDA) content was measured as an index of lipid peroxidation. The activity of Na+-K+-adenosine triphosphatase (Na+-K+-ATPase) and glutathione peroxidase (GSH-PX) was also assayed. RESULTS: The presence of rhEPO improved the survival of cultured cardiomyocytes. EPO treatment significantly decreased LDH leakage and MDA production and restored activities of Na+-K+-ATPase and GSH-PX. CONCLUSION: Pretreatment with rhEPO protects cardiomyocytes from induced injury. The beneficial effect may be related to its antioxidant properties and protection of Na+-K+-ATPase from oxidative injury.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2009-2-15.作者简介:宗刚军,主治医师,博士Email:zonggj@163.com
更新日期/Last Update: 2010-03-05