摘要
目的:探讨阿魏酸钠对幼龄大鼠心肌柔红霉素(DNR)损伤的保护作用。方法:雄性幼SD大鼠40只,随机分成4组(n=10):对照组(Control)、柔红霉素组(DNR)、阿魏酸钠干预组(DNR+SF)和阿魏酸钠单用组(SF)。采用腹腔注射DNR每周1次,连续4周,累积剂量10 mg/kg法建立未成熟心肌DNR损伤模型,于第1次注射DNR开始,每日SF(60 mg/kg)连续灌胃25 d。通过左心室插管测左心室压力及其对异丙肾上腺素反应;观察大鼠心肌超微结构改变;Western blot和RT-PCR测大鼠心肌肌钙蛋白I(c TNI)表达。结果:SF干预抑制DNR损伤引起的心率下降(P<0.05);增加大鼠左心室舒张末期压力(LVEDP)、心率(HR)、左心室最大收缩速度(LVP+dp/dtmax)和左心室最大舒张速度(LVP-dp/dtmax)对异丙肾上腺素激发的增量(P<0.01);改善心肌细胞超微结构损伤;抑制DNR损伤引起的心肌肌钙蛋白I表达下降(P<0.05)。结论:阿魏酸钠干预能减轻柔红霉素所致幼龄大鼠心力储备下降,可能与阿魏酸钠能有效逆转DNR致幼大鼠心肌收缩舒张相关蛋白c TNI表达下降有关。
Objective： To investigate the protect effects of sodium ferulate（ SF） on the daunorubicin（ DNR）-induced cardiotoxicity in juvenile rats. Methods： Forty male juvenile SD rats were randomly divided into control group（ Control）,daunorubicin group（ DNR）,sodium ferudate treatment group（ DNR ＋ SF）,sodium ferudate group（ SF）（ n = 10）. Juvenile rats were intraperitoneally treated with DNR（ 2. 5 mg / kg every week for a cumulative dose of 10 mg / kg） preparation immature myocardial injury model in presence with SF（ 60 mg / kg） oral treatment for 25 days. The left ventricular pressure and its response to isoproterenol were measured using left ventricular catheter. Rat myocardium myocardial pathology specimens and ultrastructure changes were also observed. The expression of cardiac Troponin I（ c TNI） was detected by Western blot and RT-PCR. Results： SF treatment could inhibit the decreasing of heart rates induced by DNR damage（ P〈 0. 05）; it could increase the left ventrivular end diastolic pressure（ LVEDP）,heart rate,the maximal left ventrivular systolic speed（ LVP ＋ dp / dtmax） and the maximal left ventrivular diastolic speed（ LVP-dp/dtmax） responding to isoproterenol stimulation（ P〈 0. 01）; SF also could improve the myocardial ultrastructure injuries and inhibit the decreasing of c TNI expression caused by DNR damages（ P〈 0. 05）. Conclusion： SF treatment could alleviate the decreasing of cardiac reservation induced by DNR damages in juvenile rats,which might be related to its reversing the effects on the cardiac systolic and diastolic function injuries and its inhibiting effects on the decreasing of c TNI expression caused by DNR. The mechanism of SF preventing daunorubicin-induced cardiotoxicity in juvenile rats is relevant to inhabited cardiac Troponin I expression.
出处
《中国应用生理学杂志》
CAS
CSCD
2015年第1期54-58,共5页
Chinese Journal of Applied Physiology
基金
福建省自然科学基金(2011J05069)
福建医科大学博士启动基金(2010bs007)
福建省教育厅中青年教师教育科研项目(JA14442)
关键词
阿魏酸钠
柔红霉素
心肌保护
异丙肾上腺素
sodium ferulate
daunorubicin
myocardial protection
isoproterenol
