中期因子对心肌梗死大鼠心肌胶原代谢的影响

目的探讨中期因子（Midkine,MK）对大鼠心肌胶原代谢的影响。方法 40只Wistar大鼠随机分为4组,每组10只：空白组（Control组）、伪手术组（Sham组）、梗死模型组（MI组）、MK治疗组（MI＋MK组）。通过结扎大鼠左冠状动脉前降支制作大鼠心肌梗死模型,MI＋MK组于心梗后立即给予MK心肌注射（1μg/只,分五个点注射）。4周后,各组剩余大鼠采血检测血清基质金属蛋白酶-9（MMP-9）、Ⅲ型前胶原氨基端肽（PⅢNP）水平;取心脏称重,计算全心肥厚指数;将心肌行冠状切片,行Masson染色,测定各组大鼠梗死区厚度、长度、梗死面积、梗死区及非梗死区胶原容积分数（CVF）。结果 MI组较Control、Sham组血清MMP-9、PⅢNP水平明显增高（P〈0.05）;MI＋MK组较MI组血清中MMP-9水平明显降低（P〈0.05）,PⅢNP水平明显增高（P〈0.05）;MI＋MK组较MI组梗死区厚度明显增厚,长度明显变短,梗死面积明显变小（P〈0.05）;MI＋MK组较MI组梗死区胶原容积分数明显增高（P〈0.05）,非梗死区胶原容积分数明显减低（P〈0.05）。结论 MK能够有效减轻心肌纤维化程度,其机制是通过调节心肌梗死区及非梗死区的胶原代谢来实现的。

Effect of Midkine on Myocardial collagen metabolism in Rats with Myocardial Infarction

Objective To investigate effect of Midkine on Myocardial collagen metabolism in rats with myocardial infarction（AMI）.Methods Fourty Wistar rats were randomly divided into four groups,n=10：Control group（control group）,sham-operated group（Sham group）,infarct model group（MI group）,MK treatment group（MI＋MK group）.Rat models with myocardial infarction were established by the ligation of left anterior descending coronary artery,MI＋MK group given the injection of MK immediately after myocardial infarction（1μg/rat,injection divided into five points）.Four weeks later,remaining rats in each group were test serum MMP-9,PⅢNP level;take heart weighing,calculate the whole heart hypertrophy index;Will myocardial along the shape and slice,then Masson staining,determination infarcted thickness,length,infarction area,infarcted and non infarcted collagen volume fraction（CVF） of each group rats.Results Serum of MMP-9,PⅢNP level obviously increased in the MI group than in Control and Sham groups（P0.05）;serum of MMP-9 level in the MI＋MK group decreased obviously than in the MI group（P0.05）,serum of PⅢNP level obviously increased than in the MI group（P0.05）;infarcted thickness obvious thickened,length shortens significantly,infarction area decreased significantly in the MI＋MK group than in the MI group（P0.05）;infarcted collagen volume fraction of MI＋MK group increased significantly than in the MI group（P0.05）,and noninfarcted collagen volume fraction of MI＋MK group significant decrease than in the MI group（P0.05）.Conclusion MK can effectively relieve myocardial fibrosis degree,and its mechanism is by adjusting the collagen metabolism of infarction and noninfarction area in myocardial to fulfill.