摘要
目的胃食管反流引起食管黏膜损伤的机制尚不清楚,该研究主要探讨氧化应激在小儿反流性食管炎(RE)黏膜损伤中的作用。方法对36例(年龄7个月至16岁)经胃镜检查诊断为RE的患儿,测定其食管黏膜氧化应激指标如丙二醛(MDA)、谷胱甘肽(GSH)和一氧化氮(NO)的含量和总超氧化物歧化酶(T-SOD)活力及蛋白质含量。另20例(年龄3~16岁)胃镜检查时未发现食管黏膜损伤者作为对照组。结果食管黏膜蛋白质含量在两组间差异无显著性意义(P>0.05);RE组MDA值为每毫克蛋白15.36±16.67nmol,高于对照组的7.51±6.17nmol,差异有显著性意义(P<0.01);RE组T-SOD活力每毫克蛋白为30.43±35.09U低于对照组的56.34±51.73U,差异有显著性意义(P<0.05);而GSH和NO的含量在两组间差异无显著性意义(P>0.05)。结论RE时食管黏膜MDA含量升高,SOD活力水平降低,表明氧化应激损伤在小儿食管黏膜损伤中起重要作用。
Objective To investigate the role of oxidative stress in the pathogenesis of esophageal mucosa injury in children with reflux esophagitis (RE). Methods Esophageal mucosal samples from 36 children with RE (7 months to 16 years of age) were obtained by gastroscopy. The parameters of oxidative stress, including the contents of malondialdehyde ( MDA), glutathione (GSH) and nitric oxide (NO) and total superoxide dismotase (T-SOD) activity in the esophageal mucosa as well as the protein content of the esophageal mucosa, were measured. Twenty children (3 to 16 years of age) without esophageal mucosal injury by gastroscopy served as controls. Results There was no significant difference in the protein content of the esophageal mueosa between the RE and the control groups. The content of MDA in the RE group ( 15.36 -+ 16.67 nmol/mg) was significantly higher than that in the control group (7.51 ± 6.17 nmol/mg) ( P 〈 0.01 ). The activity of T-SOD in the RE group ( 30.43 ± 35.09 U/mg) was statistically lower than that in the control group (56.34±51.73 U/mg) (P 〈0.05). No significant differences were observed in GSH and NO contents between the two groups. Conclusions The MDA content increases and the SOD content decreases in the esophageal mueosa in children with RE. This suggests that oxidative stress seems to be an important mediator in generation of esophageal mucosal injury.
出处
《中国当代儿科杂志》
CAS
CSCD
北大核心
2009年第6期425-428,共4页
Chinese Journal of Contemporary Pediatrics
基金
浙江省自然科学基金(编号Y205074)
教育部留学回国人员科研启动基金(教外司留2005.383号)
关键词
胃食管反流病
反流性食管炎
氧化应激
儿童
Gastroesophagcal reflux disease
Reflux esophagitis
Oxidative stress
Child