促心肌素1-C端肽干预大鼠心肌缺血再灌注损伤的效果

Effects of cardiotrophin 1 C-terminal peptides on rats following myocardial ischemia reperfusion injury

目的观察不同的促心肌素1-C端肽(cardiotrophin-1 C-terminal peptides,CT1C)对大鼠心肌缺血再灌注损伤后组织损伤程度的影响。方法用结扎-松解大鼠冠状动脉左后降支制作模型。正常组5鼠;缺血与再灌注组6鼠,缺血30 min后开始再灌注;缺血与再灌注后干预组8鼠,缺血30 min后开始再灌注,并腹腔注射CT1C-100μg/kg;缺血与再灌注前干预组8鼠,腹腔注射CT1C 100μg/kg,7 d后进行缺血与再灌注。实验结束前取血检测血浆一氧化氮、血清肌酸激酶和丙二醛。结果缺血与再灌注后,大鼠血一氧化氮降低(q=8.758,P<0.01),血肌酸激酶(q=14.391,P<0.01)和丙二醛浓度升高(q=11.015,P<0.01);缺血与再灌注后干预,大鼠血浆一氧化氮升高(q=14.197,P<0.01),清肌酸激酶(q=10.649,P<0.01)和丙二醛降低(q=6.167,P<0.01),但仍高于正常组(P<0.01);缺血与再灌注前干预,大鼠血浆一氧化氮浓度高于正常组(q=9.595,P<0.01),但低于后干预组(q=6.147,P<0.01),血清肌酸激酶(q=6.147,P<0.01)和丙二醛(q=10.551,P<0.01)则高于缺血与再灌注组。结论CT1C再灌注早期短期作用能减轻心肌组织损伤及氧化损伤的程度;但使用较长时间后,大鼠对缺血与再灌注的耐受力降低,组织损伤及氧化损伤的程度明显加重。

Objectives To observe the effect of cardiotrophin 1 C-terminal polypeptides （CTIC） administered pre- and post-ischemia on myocardial injury and oxidative injury after acute ischemia reperfusion in SD rats. Methods The ischemia reperfusion heart model was established by ligating/loosening the left posterior decending branch of coronary artery. Methods pairs of rats were treated with CT1 C-terminal polypeptides either before or after myocardial ischemia, and the plasma NO content and the serum CK activity and MDA content were examined. Results The plasma NO content were decreased and the serum CK activity and MDA content were increased significantly in the ischemia reperfusion group （P〈 0.01 ）, on the contrary, the plasma NO content were increased and the serum CK activity and MDA content were decreased significantly in the and post-ischemia group （P〈 0.01）. Though the serum CK activity and MDA content were more higher in pre-ischemia group than that in the ischemia reperfusion group （P 〈 0.01 ）, the plasma NO were higher than the latter, but lower than that in the post-ischemia group （P〈 0.01）. Conclusions The results suggested that the CTIC can exert myocardial protection and antioxidative ability administered after myocardial ischemia, but impair the endurance of cardioamyocytes against ischemia reperfusion injury when CTIC was used long time.