Ca2+/calmodulin-dependent protein kinase Ⅱ inhibitor K N-93 aggravates the calcium paradox-induced heart injury
10.3969/j.issn.1001-1978.2016.06.018
- VernacularTitle: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
- Author:
Lingheng KONG
;
Xiaoming GU
;
Ying NAN
;
Jiangying ZHANG
;
Na SUN
;
Juanxia ZHU
;
Jingjun ZHOU
- Publication Type:Journal Article
- Keywords:
calciumoverload;
CaMKⅡ;
KN-93;
calcium;
heart;
myocardial injury
- From:
Chinese Pharmacological Bulletin
2016;32(6):832-835,836
- CountryChina
- Language:Chinese
-
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 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.
