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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。
Objective To investigate the effect of midkine (MK) on myocardial collagen metabolism in rats. Methods Forty Wistar rats were randomly divided into 4 groups with 10 rats in each group: Control group, sham operation group, MI group and MK + MK group. Myocardial infarction models were made by ligation of the left anterior descending coronary artery in rats. Myocardial infarction was induced in the MI + MK group immediately after myocardial infarction (1 μg / dose, injected at five points). Four weeks later, serum levels of matrix metalloproteinase-9 (MMP-9) and type III procollagen aminopeptidase (PⅢNP) were determined by blood sampling in the remaining rats in each group. The heart was weighed to calculate the cardiac hypertrophy index The slices were stained with Masson. The infarct size, length, infarct area, infarct area and non-infarct area collagen volume fraction (CVF) of each group were determined. Results The levels of serum MMP-9 and PⅢNP in MI group were significantly higher than those in Control group and Sham group (P <0.05), while the levels of MMP-9 in MI + MK group were significantly lower than those in MI group (P <0.05) <0.05). The infarct size in MI + MK group was significantly thicker than that in MI group, and the infarct area was significantly shorter (P <0.05) <0.05). The volume fraction of collagen in non-infarct zone was significantly lower (P <0.05). Conclusion MK can effectively reduce the degree of myocardial fibrosis, and its mechanism is through the regulation of myocardial infarction area and non-infarction area collagen metabolism to achieve.