新生大鼠高氧肺损伤P38活化和MMP-2 mRNA表达的研究

潘涛,肖志辉

中国当代儿科杂志 ›› 2013, Vol. 15 ›› Issue (5) : 383-386.

PDF(1375 KB)
PDF(1375 KB)
中国当代儿科杂志 ›› 2013, Vol. 15 ›› Issue (5) : 383-386. DOI: 10.7499/j.issn.1008-8830.2013.05.016
论著·实验研究

新生大鼠高氧肺损伤P38活化和MMP-2 mRNA表达的研究

  • 潘涛,肖志辉
作者信息 +

Expression of P38 MAPK and MMP-2 mRNA in neonatal rats with hyperoxia-induced lung injury

  • PAN Tao, XIAO Zhi-Hui
Author information +
文章历史 +

摘要

目的:观察高氧肺损伤新生大鼠肺组织中P38-丝裂原活化蛋白激酶(P38)的活化与基质金属蛋白酶-2(MMP-2)mRNA表达水平的变化,并探讨P38的活化对MMP-2 mRNA表达的影响。方法:将36只新生Sprague-Dawley大鼠随机分为空气组、高氧组和SB203580干预组,每组12只。建立高氧肺损伤动物模型,处理组给予相应的干预。各组分别于第3天和第7天处死大鼠,常规苏木精-伊红染色,观察肺组织病理学变化;Western blot检测肺组织P38蛋白的活化水平,RT-PCR检测肺组织MMP-2 mRNA表达的变化。结果:高氧组大鼠肺组织P38的活化和MMP-2 mRNA表达水平较空气组和干预组明显增强,差异有统计学意义(P<0.01)。结论:P38在新生大鼠高氧肺损伤中活化增强,可能参与MMP-2 mRNA表达的调控。

Abstract

OBJECTIVE: To observe P38 mitogen-activated protein kinase (P38 MAPK) and matrix metalloproteinase-2 (MMP-2) mRNA expression level changes in neonatal rats with hyperoxia-induced lung injury,and to investigate the influence of P38 MAPK activation on MMP-2 mRNA expression. METHODS: Thirty-six Sprague-Dawley (SD) rats were randomly divided into three groups: air control, hyperoxia and SB203580-treated hyperoxia (n=12). The rats were sacrificed on the 3rd and 7th days and the lungs were removed. Hematoxylin-eosine staining was used to observe the pathological changes in lung tissues. RESULTS: Compared with the air and SB203580-treated groups, levels of P38 MAPK and MMP-2 mRNA significantly increased in the hyperoxia group (P<0.01). CONCLUSIONS: Expression of P38 MAPK increases in neonatal rats with hyperoxia-induced acute lung injury and this may play a role in control of the expression of MMP-2 mRNA.

关键词

P38丝裂原活化蛋白激酶 / 基质金属蛋白酶2 / 高氧 / 肺损伤 / 新生大鼠

Key words

P38 mitogen-activated protein kinase / Matrix metalloproteinase-2 / Hyperoxia / Lung injury / Neonatal rats

引用本文

导出引用
潘涛,肖志辉. 新生大鼠高氧肺损伤P38活化和MMP-2 mRNA表达的研究[J]. 中国当代儿科杂志. 2013, 15(5): 383-386 https://doi.org/10.7499/j.issn.1008-8830.2013.05.016
PAN Tao, XIAO Zhi-Hui. Expression of P38 MAPK and MMP-2 mRNA in neonatal rats with hyperoxia-induced lung injury[J]. Chinese Journal of Contemporary Pediatrics. 2013, 15(5): 383-386 https://doi.org/10.7499/j.issn.1008-8830.2013.05.016

参考文献

[1]Carvalho H, Evelson P, Sigaud S, Kwara A. Mitogen-activated protein kinases modulate H2O2-induced apoptosis in primary rat alveolar epithelial cells[J]. J Cell Biochem, 2004, 92 (3): 502-513.

[2]Yumoto H, Yamada M, Shinohara C, Schiro R, Cowan LS. Soluble products from eike nella corrodens induce cell proliferation and expression of interleukin-8 and adhesion molecules in endothelial cells via mitogen-activated protein kinase pathways[J]. Oral Microbiol Immunol, 2007, 22 (1): 36-45.

[3]Tudhope SJ, Finney-Hayward TK, Nicholson AG. Different mitogen-activated protein kinase-dependent cytokine responses in cells of the monocyte lineage[J]. J Pharm acol Exp Ther, 2008, 324 (1): 306-312.

[4]Elkington PT, Emerson JE, Lopez-Pascua LD, Hunter PR. Mycobacteriumtuberculosis up-regulates matrix metalloproteinase-1 secretion fromhuman airway epithelial cells via p38 MAPK switch[J]. J Immunol, 2005, 175 (8): 5333-5340.

[5]胡良冈, 钱燕, 龚永生.SPF级新生大鼠高氧肺损伤模型的建立[J].中国实验动物学报,2008,16(6):441-443.

[6]Obat T, Brown GE, Yaffe MB, Gaston MA. MAPkinase pathway activated by stress the p38 MAPK pathway[J]. Critical Care Med, 2000, 28(4): 67-77.

[7]Romashko J, Horowitz S, Franek WR. MAPK pathways mediatehy peroxia-induced oncotic cell death in lung epithelial cells[J]. Free Radic Biol Med, 2003, 35 (8): 978-993.

[8]Sigaud S, Evelson P, Gonzalez-Flecha B, Alland D. H2O2-induced proliferation of primary alveolar epithelial cells ismediated by MAP kinases[J]. Antioxid Redox Signal, 2005, 7 (1-2): 6-13.

[9]Kuo WH, Chen JH, Lin HH. Induction of apoptosis in the lung tissue from rats exposed to cigarette smoke involves p38/JNK MAPK pathway[J]. Chem Biol Interact, 2005, 155 (1-2): 31-42.

[10]Wang W, Wei W, Ning Q. Effect of intra-amniotic endotoxin priming plus hyperoxia exposure on the expression of vascular endothelial growth factor and its receptors in lungs of preterm newborn rats[J]. Chin J Pediatr, 2007, 45 (7): 533-538.

[11]李文斌,常立文,容志惠.高氧、维甲酸对早产鼠肺组织基质金属蛋白酶-2、-9及特异性组织抑制物-1、-2 表达的影响[J]. 临床儿科杂志,2007,25(6):497-503.

[12]Pillinger MH, Marjanouic N, Kim SY, Fine PE. Matrixmetalloproteinase secretion by gastric ep ithelial cells is regulated by Eprostaglandins and MAPKs[J]. J Biol Chem, 2005, 280 (11): 9973-9979.

[13]Park MJ, Park IC, Hur JH, Kalkut GE. Modulation of phorbolester-induced regulation of matrix-metalloproteinases and tissue inhibitors of metalloproteinases by SB203580, a specific inhibitor of p38 mitogen-activated protein kinase[J]. J Neurosurg, 2002, 97 (1): 112-118.

[14]Nee LE, McMorrow T, Campbell E. TNF-alpha and IL-1beta-mediated regulation of MMP-9 and TIMP-1 in renalproximal tubular cells[J]. Kidney Int, 2004, 66 (4): 1376-1386.


PDF(1375 KB)

Accesses

Citation

Detail

段落导航
相关文章

/