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首页> 外文期刊>Life sciences >Roles of pro-angiogenic and anti-angiogenic factors as well as matrix metalloproteinases in healing of NSAID-induced small intestinal ulcers in rats
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Roles of pro-angiogenic and anti-angiogenic factors as well as matrix metalloproteinases in healing of NSAID-induced small intestinal ulcers in rats

机译：促血管生成和抗血管生成因子以及基质金属蛋白酶在NSAID诱导的大鼠小肠溃疡愈合中的作用

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Aims We examined changes in the expression of a pro-angiogenic factor, vascular endothelial growth factor (VEGF), and an anti-angiogenic factor, endostatin, as well as matrix metalloproteinase (MMP)-2 and MMP-9 in the rat small intestine after administration of indomethacin and investigated the roles of these factors in the healing of indomethacin-induced small intestinal ulcers. Main methods Male SD rats were given indomethacin (10 mg/kg) p.o. and euthanized at various time points (3-24 h and 2-7 days) after the administration. To impair the healing of these lesions, low-dose of indomethacin (2 mg/kg) was given p.o. once daily for 6 days starting 1 day after ulceration. Levels of VEGF, endostatin, MMP-2 and MMP-9 were determined by Western blotting. Key findings The expression of both VEGF and endostatin was upregulated after the ulceration. Repeated administration of low-dose indomethacin impaired the ulcer healing with a decrease of VEGF expression and a further increase of endostatin expression, resulting in a marked decrease in the ratio of VEGF/endostatin expression. The levels of MMP-2 and MMP-9 were both significantly increased after the ulceration, but these responses were suppressed by the repeated indomethacin treatment. The healing of these ulcers was significantly delayed by the repeated administration of MMP inhibitors such as ARP-101 and SB-3CT. Significance The results confirm the importance of the balance between pro-angiogenic and anti-angiogenic activities in the healing of indomethacin-induced small intestinal damage and further suggest that the increased expression of MMP-2 and MMP-9 is another important factor for ulcer healing in the small intestine.
机译：目的我们检查了大鼠小肠中促血管生成因子，血管内皮生长因子（VEGF）和抗血管生成因子，内皮抑素以及基质金属蛋白酶（MMP）-2和MMP-9的表达变化服用消炎痛后，研究了这些因素在消炎痛诱导的小肠溃疡愈合中的作用。主要方法雄性SD大鼠口服给予消炎痛（10 mg / kg）。在给药后的各个时间点（3-24小时和2-7天）实施安乐死。为了损害这些病变的愈合，口服低剂量的消炎痛（2 mg / kg）。从溃疡后1天开始，每天一次，连续6天。通过蛋白质印迹法测定VEGF，内皮抑素，MMP-2和MMP-9的水平。主要发现溃疡后VEGF和内皮抑素的表达均上调。低剂量消炎痛的反复给药会损害溃疡，导致VEGF表达降低，内皮抑素表达进一步增加，从而导致VEGF /内皮抑素表达比率显着降低。溃疡后，MMP-2和MMP-9的含量均显着增加，但是通过反复的消炎痛治疗抑制了这些反应。这些溃疡的愈合被MMP抑制剂（如ARP-101和SB-3CT）的重复给药大大延迟了。意义该结果证实了促血管生成和抗血管生成活性之间的平衡在消炎痛诱导的小肠损伤的愈合中的重要性，并进一步表明MMP-2和MMP-9表达的增加是溃疡愈合的另一个重要因素在小肠里。

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