论文部分内容阅读
目的探讨基质细胞蛋白Tenascin-C在慢性免疫性心肌炎小鼠心室重构中的作用。方法SPF级BALB/c小鼠75只,随机分为实验组(45只)和对照组(30只)。以心肌肌球蛋白重链614-629位多肽与完全弗氏佐剂的混合液免疫实验组小鼠建立实验性自身免疫性心肌炎(EAM)模型,对照组注射相同量磷酸盐缓冲液与完全弗氏佐剂的混合液。分别在不同时间点(21、75、120d)观察小鼠心肌的病理性重构情况,采用Western blotting检测心肌Tenascin-C的表达,放射免疫法测定血清Ⅲ型胶原氨基末端肽(PⅢNP)含量,并分析两者之间的相关性。结果21d时,实验组小鼠心肌炎性浸润明显,间质出现少量胶原沉积;至75、120d时,实验组小鼠心肌炎性浸润显著减少,间质胶原沉积更加明显。实验组在各时间点血清PⅢNP含量及心肌Tenascin-C蛋白表达均显著高于对照组(P<0.01),且随着病程进展而增加(P<0.01)。心肌Tenascin-C蛋白的表达与血清PⅢNP含量呈正相关(r=0.893,P<0.01)。结论Tenascin-C参与了心肌炎小鼠心肌纤维化及心室重构的进展,可能在心肌疾病的发生发展中具有重要作用。
Objective To investigate the role of stromal cell protein Tenascin-C in ventricular remodeling in mice with chronic immune myocarditis. Methods Seventy five SPF BALB / c mice were randomly divided into experimental group (n = 45) and control group (n = 30). The model of experimental autoimmune myocarditis (EAM) was established by immunizing experimental mice with a mixture of cardiac myosin heavy chain 614-629 polypeptide and complete Freund’s adjuvant. The control group was injected with the same amount of phosphate buffered saline A mixture of adjuvants. The myocardial remodeling was observed at different time points (21, 75 and 120 days). The expression of Tenascin-C in myocardium was detected by Western blotting. The content of serum type Ⅲ collagen aminoterminal peptide (PⅢNP) And analyze the correlation between the two. Results At 21 days, myocardium inflammatory infiltration in the experimental group was obvious and a small amount of collagen deposition appeared in the interstitium. At 75 and 120 days, myocardial infiltration in the experimental group was significantly reduced and interstitial collagen deposition was more obvious. At each time point, the level of PⅢNP and the expression of Tenascin-C in myocardial tissue in experimental group were significantly higher than those in control group (P <0.01), and increased with the course of disease (P <0.01). The expression of myocardial Tenascin-C protein was positively correlated with the level of PⅢNP in serum (r = 0.893, P <0.01). Conclusion Tenascin-C is involved in the progression of myocardial fibrosis and ventricular remodeling in myocarditis mice and may play an important role in the development of myocardial disease.