...
首页> 外文期刊>Hepato-gastroenterology. >mRNA expression of inducible nitric oxide synthase, endothelial nitric oxide synthase and vascular endothelial growth factor in esophageal mucosa biopsy specimens from patients with reflux esophagitis.
【24h】

mRNA expression of inducible nitric oxide synthase, endothelial nitric oxide synthase and vascular endothelial growth factor in esophageal mucosa biopsy specimens from patients with reflux esophagitis.

机译:返流性食管炎患者食管黏膜活检标本中诱导型一氧化氮合酶,内皮型一氧化氮合酶和血管内皮生长因子的mRNA表达

获取原文
获取原文并翻译 | 示例
           

摘要

BACKGROUND/AIMS: Nitric oxide (NO) production is elevated in the intestine and may contribute to intestinal injury during inflammation. However, how the expression of inducible NO synthase (iNOS) mRNA and endothelial NO synthase (eNOS) mRNA in the esophageal mucosa contribute to mucosal damage caused by reflux esophagitis remains unknown. Since vascular endothelial growth factor (VEGF) exerts its action on microcirculation, contributing to angiogenesis and inflammation, we examined the role of VEGF together with iNOS and eNOS on development of reflux esophagitis. METHODOLOGY: The mRNA expression levels of iNOS, eNOS and VEGF were measured in biopsy specimens from 25 patients with reflux esophagitis, using TaqMan PCR and reverse transcription PCR. RESULTS: The expression of iNOS mRNA in the esophageal mucosa increased parallel to the severity of the esophagitis. There were no significant differences between both eNOS and VEGF mRNA expression levels and the severity of the esophagitis. The existence of gastric mucosal atrophy, hiatus hernia, therapy and Helicobacter pylori infection did not affect the levels of mRNA expression. CONCLUSIONS: The accumulation of NO, produced by iNOS, was considered to be related to the exacerbation of reflux esophagitis. Therapeutic intervention that reduces NO production may thus be of use in preventing development of esophageal mucosal injury in patients with reflux esophagitis.
机译:背景/目的:一氧化氮(NO)的产生在肠中增加,并可能在炎症过程中导致肠损伤。然而,在食管粘膜中诱导型一氧化氮合酶(iNOS)mRNA和内皮型一氧化氮合酶(eNOS)mRNA的表达如何导致由反流性食管炎引起的粘膜损害尚不清楚。由于血管内皮生长因子(VEGF)在微循环中发挥作用,有助于血管生成和炎症,因此我们研究了VEGF与iNOS和eNOS一起在反流性食管炎发展中的作用。方法:采用TaqMan PCR和逆转录PCR技术检测25例反流性食管炎患者的活检标本中iNOS,eNOS和VEGF的mRNA表达水平。结果:食管黏膜中iNOS mRNA的表达与食管炎的严重程度平行。 eNOS和VEGF mRNA表达水平与食管炎严重程度之间无显着差异。胃粘膜萎缩,裂孔疝,治疗和幽门螺杆菌感染均不影响mRNA表达水平。结论:iNOS产生的NO的积累被认为与反流性食管炎的恶化有关。因此,减少NO产生的治疗性干预可用于预防反流性食管炎患者食道粘膜损伤的发展。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号