Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Department of Cardiology, Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453000, P.R. China.
Mol Med Rep. 2018 Mar;17(3):3519-3526. doi: 10.3892/mmr.2017.8347. Epub 2017 Dec 27.
The present study aimed to investigate kinetic alterations of collagen and elastic fibres and their association with cardiac function in the acute myocardial infarction (AMI) heart. AMI was generated in Sprague-Dawley rats by ligation of the left anterior descending coronary artery. Cardiac function was determined using B‑ultrasonography, AMI was verified using histopathology. The kinetics of collagen type I/III and elastic fibre were evaluated using immunohistochemistry and western blotting at 1 week (1 w), 2 weeks (2 w), 3 weeks (3 w) and 4 weeks (4 w) post‑AMI. Cardiac function was decreased by 78, 70, 50 and 38% at weeks 1, 2, 3 or 4 post‑AMI, respectively, compared with the normal heart. Elastic fibre was decreased gradually, demonstrating alterations of 2, 77, 86 or 97% reduction, respectively, at weeks 1, 2, 3 or 4 in the AMI heart. Collagen I fibre was increased 1.4‑, 1.5‑, 2.9‑ or 3.9‑fold at weeks 1, 2, 3 or 4 respectively, compared with the normal heart. Similarly, collagen III was increased 1.2‑, 1.7‑, 2.8‑ or 3.9‑fold, following AMI. Kinetics of increased collagen I/III, in combination with decreased elastic fibre in infarcted area following AMI, provided evidence that compromised cardiac function following AMI was due to graduate wound healing/scar formation in the infarcted zone, increased stiffness and reduced flexibility of the heart.
本研究旨在探讨胶原和弹性纤维的动力学改变及其与急性心肌梗死（AMI）心脏心功能的关系。通过结扎左前降支冠状动脉在 Sprague-Dawley 大鼠中产生 AMI。使用 B 超心动图测定心功能，通过组织病理学验证 AMI。在 AMI 后 1 周（1w）、2 周（2w）、3 周（3w）和 4 周（4w），通过免疫组化和 Western blot 评估 I/III 型胶原和弹性纤维的动力学。与正常心脏相比，AMI 后 1、2、3 或 4 周，心脏功能分别降低了 78%、70%、50%和 38%。弹性纤维逐渐减少，AMI 心脏分别减少了 2%、77%、86%或 97%。I 型胶原纤维分别增加了 1.4 倍、1.5 倍、2.9 倍或 3.9 倍，与正常心脏相比，分别在 1、2、3 或 4 周时。同样，III 型胶原增加了 1.2 倍、1.7 倍、2.8 倍或 3.9 倍。在 AMI 后，I/III 型胶原的动力学增加，结合梗死区弹性纤维减少，表明 AMI 后心脏功能受损是由于梗死区逐渐愈合/瘢痕形成，导致心脏僵硬增加和柔韧性降低。
