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目的:探讨糖尿病并发心肌梗死(MI)对大鼠心肌中神经生长因子(NGF)的表达及交感神经再生重构的影响。方法:将实验大鼠分为正常对照组、糖尿病对照组、MI对照组及糖尿病MI组,从各组大鼠的左心室梗死周边、室间隔和右心室取材,通过免疫组化染色并结合计算机图像处理技术,对心肌中NGF蛋白表达及交感神经支配进行对比分析。结果:与正常对照组及糖尿病心梗组比较,MI对照组的NGF表达均增加(均P<0.05),交感神经支配密度也均明显增加(均P<0.01),并且二者在梗死周边、室间隔及右心室3个部位的表达存在相关性(均P<0.05),糖尿病对照组的NGF表达均降低(P<0.05,P<0.01),交感神经支配密度分别为无明显差异及明显降低(P<0.01)。结论:糖尿病可抑制心肌细胞表达NGF,但却可促进MI后交感神经的过度再生与重构。推测糖尿病条件下,NGF并非交感神经再生重构的决定因素,尚存在其他途径对交感神经再生及重构进行调节。
Objective: To investigate the effects of diabetes complicated with myocardial infarction (MI) on the expression of nerve growth factor (NGF) and sympathetic nerve regeneration in rats. Methods: The experimental rats were divided into normal control group, diabetic control group, MI control group and diabetic MI group. The left ventricular infarction peripheral, interventricular septum and right ventricle of the rats in each group were harvested and analyzed by immunohistochemistry and computer Image processing technology, myocardial NGF protein expression and sympathetic innervation comparative analysis. Results: Compared with normal control group and diabetic myocardial infarction group, NGF expression in MI control group increased (all P <0.05) and sympathetic innervation density also increased significantly (both P <0.01) (P <0.05). The expression of NGF in diabetic control group was decreased (P <0.05, P <0.01), and there was no significant difference in the density of sympathetic innervation (P <0.01). Conclusion: Diabetes mellitus can inhibit the expression of NGF in cardiomyocytes, but it can promote the over-regeneration and remodeling of sympathetic nerve after MI. Speculated that diabetic conditions, NGF is not a determinant of sympathetic nerve regeneration, there are other ways to regulate sympathetic nerve regeneration and remodeling.