Ⅱ型糖尿病大鼠心肌梗死后交感神经重构与神经生长因子(NGF)的表达改变 |
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引用本文: | 刘野,路军,刘雄涛,丁璐,滕继伟,郑强荪.Ⅱ型糖尿病大鼠心肌梗死后交感神经重构与神经生长因子(NGF)的表达改变[J].心脏杂志,2010,22(3):347-350. |
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作者姓名: | 刘野 路军 刘雄涛 丁璐 滕继伟 郑强荪 |
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作者单位: | 1.第四军医大学唐都医院心内科,陕西 西安 710038;2.解放军第208医院心内科,吉林 长春 130062 |
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摘 要: | 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P0.05),交感神经支配密度也均明显增加(均P0.01),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P0.05),糖尿病对照组的NGF表达均降低(P0.05,P0.01),交感神经支配密度分别为无明显差异及明显降低(P0.01)。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。
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关 键 词: | 糖尿病 心肌梗死 交感神经 神经生长因子 大鼠 |
收稿时间: | 2009-05-04 |
Expression of nerve growth factor and sympathetic neural remodeling after myocardial infarction in type II diabetic rats |
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Abstract: | AIM: To explore the alteration of the expression of nerve growth factor (NGF) and sympathetic neural remodeling after myocardial infarction in type II diabetic rats. METHODS: Samples were obtained from the peri-infarcted area, ventricular septum and right ventricle (RV) in infarcted diabetic rats. Using immunohistochemistry and computerized image-processing technique, expressions of NGF protein and sympathetic innervation were examined in different groups (blank, diabetic, infarcted, and infarcted diabetic, respectively). RESULTS: In the diabetic group, expressions of NGF protein were lower than those in the blank group (P<0.05) and those in the infarcted diabetic group (P<0.01). The density of sympathetic nerves was also lower than in the infarcted diabetic group (P<0.01). In the infarcted group, expressions of NGF protein and density of sympathetic nerves were both higher than in the blank group (P<0.05, P<0.01) and those in the infarcted diabetic group (P<0.05, P<0.01). NGF protein expression was correlated with sympathetic innervation in the peri-infarcted area, RV and septum in infarcted group (P<0.05). CONCLUSION: Diabetes mellitus decreases the expression of NGF protein in cardiomyocytes but increases sympathetic reinnervation and hyperinnervation, indicating that it may not be NGF but some other factor that plays a crucial role in post-infarct neural remodeling. |
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