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钙/钙调蛋白依赖性蛋白激酶Ⅱ抑制剂K N-93加重大鼠离体心脏钙超载损伤

孔令恒 顾晓明 南瑛 张建英 孙娜 朱娟霞 周京军

中国药理学通报2016,Vol.32Issue(6):832-835,836,5.
中国药理学通报2016,Vol.32Issue(6):832-835,836,5.DOI:10.3969/j.issn.1001-1978.2016.06.018

钙/钙调蛋白依赖性蛋白激酶Ⅱ抑制剂K N-93加重大鼠离体心脏钙超载损伤

Ca2+/calmodulin-dependent protein kinase Ⅱ inhibitor K N-93 aggravates the calcium paradox-induced heart injury

孔令恒 1顾晓明 2南瑛 3张建英 1孙娜 3朱娟霞 1周京军1

作者信息

  • 1. 西安医学院基础部生理学教研室,陕西西安 710021
  • 2. 第四军医大学基础部生理学教研室,陕西西安 710032
  • 3. 第四军医大学基础部生理学教研室,陕西西安 710032
  • 折叠

摘要

Abstract

Aim ToinvestigatetheeffectsofCa2+/calmodulin-dependent protein kinase Ⅱ inhibitor KN-93 on calcium overload-induced heart injury.Methods Thirty-twoisolatedratheartswererandomlydivided into the control group,KN-93 control group,calcium paradox group,and calcium paradox with KN-93 treat-ment group.Left ventricular pressure were recorded, and the heart function was evaluated by the left ventric-ular end-diastolic pressure (LVEDP ) and developed pressure (LVDP).Coronary flow (CF)were collect-ed,and lactate dehydrogenase (LDH)content was de-termined.Triphenyltetrazolium chloride staining was usedtomeasuretheinfarctsize.Results Compared with the control group,KN-93 at 2. 5 μmol·L-1 had&nbsp;no effects on coronary flow,cardiac performance and cell death at the end of perfusion in normal rats (P>0. 05 );The hearts of calcium paradox exhibited a de-crease in LVDP and CF,meanwhile an increase in LV-EDP,LDH,and infarct size of 18 ±7. 2% (P <0. 01).2. 5 μmol·L-1 KN-93 further increased the levels of LVEDP,LDH and infarct size (P<0. 01)in Ca2+paradoxical hearts,while it provoked the decline intheCFandLVDP(P<0.01).Conclusion The data demonstrates that KN-93 aggravates heart injury in calcium paradox,it also suggests that CaMKⅡ is in-volved in the Ca2+overload-induced heart injury.

关键词

钙超载/钙/钙调蛋白依赖性蛋白激酶Ⅱ/KN-9 3/钙离子/心脏/心肌损伤

Key words

calciumoverload/CaMKⅡ/KN-93/calcium/heart/myocardial injury

分类

医药卫生

引用本文复制引用

孔令恒,顾晓明,南瑛,张建英,孙娜,朱娟霞,周京军..钙/钙调蛋白依赖性蛋白激酶Ⅱ抑制剂K N-93加重大鼠离体心脏钙超载损伤[J].中国药理学通报,2016,32(6):832-835,836,5.

基金项目

国家自然科学基金资助项目(No.31371181);陕西省科技厅项目(No 2014JM2-8164);西安医学院学科建设经费资助 ()

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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