Chinese Medical E-ournals Database

Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition) ›› 2009, Vol. 05 ›› Issue (01): 23 -28. doi: 10.3877/cma.j.issn.1673-5250.2009.01.108

Original Article

Correlation Study Between the Myocardial Anoxia Ischemia Reperfusion Injury and Myocardium Remodeling in Asphyxiated Newborn Rats.

Shu–zhen XU, Cai–xia WANG, Wei ZHAO, Jian–fang CHU   

  1. Department of Pediatrics, Qingdao Municipal Hospital, Qingdao 266011, China
  • Published:2009-02-01
Objective

To observe the expression of matrix metalloproteinases (MMPs) and transforming growth factor-β1 (TGF-β1) and their effectiveness on myocardial repairing and remodeling after anoxia ischemia reperfusion injury in rats.

Methods

The anoxia ischemia reperfusion injury animal model was set up in this study. Sixty Wistar rats were randomly divided into 4 groups: the group A, B, C (at the first day, the seventh day and the fourteenth day after the myocardial anoxia ischemia reperfusion injury) and the control group(without any asphyxia treatment)(15 rats for each group). The blood serum cardiac troponin Ⅰ (cTnⅠ) was measured by the rapid quantifying. Masson staining was used to study the collagen volume fraction (CVF), and myocardial histopathological integration was tested by the HE staining. The myocardial matrix metalloproteinase-3, -9 activities was measured by the immunohistochemical assay, and the transforming growth factor-β1 expression of myocardium were measured by the immunohistochemistry assay and semiquantitative analysis.

Results

Serum cardiac troponin Ⅰ provisionality raised, the level of the group A were obviously higher than those of the control group (P<0.01), but the level of the group B and C declined (P>0.05); matrix metalloproteinase-3 activity in the group A, B and C were significantly higher than those of the control group, reaching a peak on the group B (P<0.05). The metalloproteinase-9 activity in the group A, B and C were significantly higher than those of the control group (P<0.05). Collegen volume fractions were gradually increased after asphyxia(P>0.05, P<0.05, P<0.05, respectively) and the group C reached the highest level. The expression of transforming growth factor-β1 enhanced by the change of the time(P>0.05, P<0.01, P<0.01, respectively). Collegen volume fractions were positively correlated with transforming growth factor-β1 (r=0.574, P<0.01). Matrix metalloproteinase-3, -9 activities positively correlated with collegen volume fractions (r=0.482, 0.679; P<0.05).

Conclusion

There has anoxia ischemia reperfusion injury in rats myocardium. After the asphyxia, the matrix metalloproteinase-3, -9 activities are activited and the expression of transforming growth factor-β1 are enhanced, myocardial collagens increase. Matrix metalloproteinase-3, -9, transforming growth factor-β1 may relate with the myocardial remodeling after the anoxia ischemia reperfusion injury.

图1 MMP-3免疫组化阳性表达(S-P×100)
图2 MMP-9免疫组化阳性表达(S-P×200)
图3 HE染色心肌细胞肥大
图4 HE染色胶原增生
图5 免疫组化TGF-β1阳性
1 Iwai T, Hara A, Niwa M, et al. Temporal profile of nuclear DNA fragmentation in situ in gerbil hippocampus following transient forebrain ischemia. Brain Res, 1995, 671(2): 305–308.
2 Dong EB, Ran LR, Feng ZQ, et al. Protection effect of sheng mai injection on postasphyxied brain damage. Chin J Child Health Care, 1998, 6(1): 32–34.[董文斌,冉隆瑞,冯志强,等.生脉注射液对窒息后脑损伤保护作用的研究. 中国儿童保健杂志,1998, 6(1): 32–34.]
3 Tyagi SC, Kumar SG, Haas SJ, et al. Post–transcriptional regulation of extracellular matrix metalloproteinase in human heart end–stage failure secondary to ischemic cardiomyopathy. J Mol Cell Cardiol, 1996, 28(7): 1415–1428.
4 Hozumi A, Nishimura Y, Nishiuma T, et al. Induction of MMP–9 in normal human bronchial epithelial cells by TNF–alpha via NF–kappa B–mediated pathway. Am J Physiol Lung Cell Mol Physiol, 2001, 281(6): L1444–1452.
5 Alexander JP, Acott TS. Involvement of protein kinase C in TNFalpha regulation of trabecular matrix metalloproteinases and TIMPs. Invest Ophthalmol Vis Sci, 2001, 42(12): 2831–2838.
6 Ducharme A, Franz S, Aikawa M, et al. Targeted deletion of matrix metalloproteinase–9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest, 2000, 106: 55–62.
7 Tyagi SC, Kumar SG, Haas SJ, et al. Post–transcriptional regulation of extracellular matrix metalloproteinase in human heart end–stage failure secondary to ischemic cardiomyopathy. J Mol Cell Cardiol, 1996, 28(7): 1415–1428.
8 Seeland U, Haeuseler C, Hinrichs R, et al. Myocardial fibrosis in transforming growth factor–beta 1(TGF–beta 1) transgenic mice is associated with inhibition of interstitial collagenase. Eur J Clin Invest, 2002, 32(5): 295–303.
9 Thomas CV, Coker ML, Zellner JL, et al. Increased matrix metalloproteinase activity and selective upregulation in LV myocardium from patients with end–stage dilated cardiomyopathy. Circulation, 1998, 97(17): 1708–1715.
10 Spinale FG, Coker ML, Bond BR, et al. Myocardial matrix degradation and metallopro–teinase activation in the failing heart: A potential therapeutic target. Cardiovasc Res, 2000, 46(2):225–238.
11 Luo HL, He ZY, Feng B, et al. Clinical research on bFGF and TGF–β1 expression and heart hypertrophy. J Clin Cardiol, 2001, 17(2): 83–84. [罗惠兰,何作云,冯兵,等. 碱性成纤维细胞生长因子和转化生长因子β1表达与心肌肥大的研究. 临床心血管病杂志,2001, 17(2): 83–84.]
12 Danielsen CC, Wiggers H, Andersen HR. Increased amounts of collagenase and gelatinase in porcine myocardium following ischemia and reperfusion. J Mol Cell Cardiol, 1998, 30(7): 1431–1442.
13 Cheung PY, Sawicki G, Wozniak M, et al. Matrix metalloproteinase–2 contributes to ischemia–reperfusion injury in the heart. Circulation, 2000, 101(15):1833–1839.
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