异丙肾上腺素诱导的大鼠肥厚心肌组织中Ⅰ、Ⅲ型胶原蛋白的表达

Expression of collagen Ⅰ and Ⅲ in the hypertrophic myocardial tissue of the rat heart treated by isoproterenol

目的探讨Ⅰ、Ⅲ型胶原在肥厚心肌组织中的变化特征。方法 SD大鼠60只,分为对照组和实验组,两组分别再分为1、4、8周组,每组10只。对照组背部皮下注射生理盐水4ml/(kg.d);实验组背部皮下注射异丙肾上腺素4mg/(kg.d)。两组分别注射1、4、8周,然后测定各组大鼠体重(BW)、心脏湿重(HW)、左室湿重(LVW),计算出HW/BW、LVW/BW;心肌组织冷冻切片,利用图像分析软件,测量心肌细胞横径(TDM)和心肌细胞截面积(CA)。免疫组织化学法检测各组心肌组织Ⅰ、Ⅲ型胶原的表达。Western blotting方法检测心肌肥厚大鼠心肌Ⅰ、Ⅲ型胶原蛋白表达及其含量。结果免疫组织化学结果显示,注射异丙肾上腺素1周后,Ⅰ和Ⅲ型胶原蛋白表达明显增加,4周后有所下降。Western blotting结果显示,实验各组Ⅰ型和Ⅲ型胶原蛋白表达均多于对照组(P<0.01);实验1周时Ⅰ型和Ⅲ型胶原蛋白表达量最高,4周和8周均下降。实验4周和8周组与1周组比较差异有统计学意义(P<0.05)。结论心肌肥厚发生1周左右是Ⅰ、Ⅲ型胶原增加的高峰期,以后趋于稳定。心肌肥厚主要引起胶原量的变化,不破坏胶原纤维的网络结构。

Objective To investigate changes of collagen Ⅰ and Ⅲ in hypertrophic myocardial tissue of the rat. Methods Sixty SD rats were divided into control groups and model groups. Each group was further subdivided into sub- groups of 1- week, 4- week and 8- week groups, 10 rats in each group. The rat of the model group was injected subcutaneously with isop roterenol at the dose of 4mg/（kg. d） for 1 week,4 and 8 weeks, respectively. In the control group,isoproterenol was replaced with saline. The body weight （BW） , heart humid weight （HW） , left ventricular humid weight （LVW） of each rat were measured. Myocardiac tissues were excised for cryostat section. The myocardiac transverse diameter（MTD） ,myocardiac section area（MYOR） were measured with an image analysis system. Immunohistochemistry and Western blotting were used to measure the protein concentrations for collagen Ⅰ and Ⅲ. Results The intensities for the collagen I and m staining were significantly higher in iso-injection 1-week group than those in 4-week group. The results of Western blotting showed that the expression of collagen Ⅰ and Ⅲ proteins in model groups were higher than that in the control groups（P 〈 0.01 ）. Collagen Ⅰ and Ⅲcontents increase at 1-week treatment for cardiac hypertrophy and then regress to a stable state. Conclusion Myocardial hypertrophy will lead mainly to the change of collagen protein contents but do not destroy the morphological collagen network.