幽门螺杆菌感染时胃黏膜一氧化氮合酶活性和脂质过氧化  

Gastric mucosal nitric oxide synthase activity and lipid peroxidation in Helicobacter pylori infection

作　　者：赵逵[1] 商黔惠[1] 马淑玉[1] 史济经[1] 庹必光[1] 何毅[1] 

机构地区：[1]遵义医学院附属医院消化内科

出　　处：《中华内科杂志》1998年第7期455-458,共4页Chinese Journal of Internal Medicine

基　　金：卫生部青年科学基金

摘　　要：目的探讨幽门螺杆菌（Ｈｐ）感染时胃黏膜一氧化氮（ＮＯ）与脂质过氧化损伤的关系。方法测定１２名正常对照、１４例Ｈｐ阴性、２２例Ｈｐ阳性慢性胃炎和２７例Ｈｐ阳性消化性溃疡患者胃窦黏膜ＮＯ合酶（ＮＯＳ）活性、铜锌超氧化物歧化酶（ＣｕＺｎＳＯＤ）和丙二醛（ＭＤＡ）含量。结果Ｈｐ阳性胃炎和溃疡患者ＮＯＳ活性和ＭＤＡ含量显著高于、ＣｕＺｎＳＯＤ含量低于Ｈｐ阴性者，溃疡ＮＯＳ活性高于Ｈｐ阳性胃炎；Ｈｐ阳性患者ＮＯＳ活性与胃炎积分和ＭＤＡ呈正相关，ＣｕＺｎＳＯＤ与ＭＤＡ呈负相关；ＮＯＳ抑制剂ＬＮＭＭＡ可显著抑制Ｈｐ阳性患者ＮＯＳ活性，而乙二醇双四乙酸对ＮＯＳ活性无影响。Ｈｐ根除后，胃炎积分、ＮＯＳ活性和ＭＤＡ含量均显著下降、ＣｕＺｎＳＯＤ含量增高。结论Ｈｐ感染时胃黏膜ＮＯＳ活性增高与来源于炎症细胞产生的诱生型ＮＯＳ增多有关；Objective To study the relationship between nitric oxide (NO) and reactive oxygen metabolite (ROM) damage in gastric mucosa of patients with Helicobacter pylori (Hp) infection. Methods NO synthase activity, copper zinc superoxide dismutase (Cu Zn SOD) and malondialdehyde (MDA, as a measure of ROM mediated lipid damage) levels were measured by using the reaction of NO with oxyhaemoglobin with radioimmunoassay. These were measured with the supernatants of homogenised antral mucosal biopsy specimens taken from 12 Hp negative normal controls, 14 Hp negative and 22 positive patients with chronic active gastritis in a similar spectrum of Rauws's microscopic scores and 27 Hp positive patients with active peptic ulcer. Results NO synthase activity and MDA levels were significantly higher and Cu Zn SOD levels lower in Hp positive gastritis and peptic ulcer patients than those in Hp negative gastritis patients and normal subjects. NO synthase activity in peptic ulcer patients was also higher than that in Hp positive gastritis patients. In Hp positive patients, NO synthase activity showed a positive correlation with Rauws's gastritis scores and MDA levels ( r =0 674, P <0.01; r =0.656, P <0.01 respectively; n =49), whereas Cu Zu SOD levels had a negative correlation with MDA levels ( r =-0 527, P <0.01). The enhanced NO synthase activity was significantly inhibited by arginine analogue L NMMA but not by calcium chelating agent EGTA in biopsy specimens of 12 Hp positive patients. Gastritis scores, NO synthase activity and MDA levels were markedly decreased and Cu Zn SOD levels increased in 20 patients after successful eradication of Hp, but there was no change in 16 patients with unsuccessful eradication of Hp. Conclusion It is suggested that the enhanced NO synthase activity expressing the inducible isoform is probably derived from mucosal inflammatory leukocytes and NO as a free radical may be involved in the pathogenetic mechanisms of gastric mucosal ROM damage in Hp infection, s

关 键 词：一氧化氮 超氧化物歧化酶 胃粘膜 幽门螺杆菌 

分 类 号：R573.02[医药卫生—消化系统]