Hp对慢性萎缩性胃炎内皮素及一氧化氮水平影响的实验与临床研究

Changes of nitricoxide and endothelin in Helicobacter pylori associated chronic atrophic gastritis before and after eradication: an experimental and clinical study

目的:试图通过实验与临床研究观察Hp根除前后慢性萎缩性胃炎(CAG)NO和ET水平的改变,从这一角度出发探讨Hp相关CAG的发病机制.方法:(1)实验研究:采用SS1Hp菌株,3%水杨酸钠、5%乙醇,5mmol/L去氧胆酸钠灌胃,加以饥饱失常,制作Hp相关CAG大鼠模型.模型大鼠随机分成3组:(a)Hp根除组:根除Hp三联(德诺、阿莫西林、甲硝唑)治疗2wk.(b)模型自然恢复组:采用蒸馏水灌胃.(c)正常对照组:正常大鼠.治疗结束后3mo处死全部大鼠,进行Hp、病理组织学检查及血清一氧化氮(NO)、内皮素(ET)含量测定.(2)临床研究:选择Hp阳性CAG患者42例,Hp阴性CAG患者25例,Hp阳性慢性浅表胃炎(CSG)21例,分别进行Hp、病理组织学检查及血中NO和ET测定.结果:实验CAG模型中,Hp根除组血清NO、ET含量[(3672±1845)ng/ml,(181.14±22.5)×10-3ng/ml]较模型自然恢复[(5887±1896)ng/ml,(211.67±34.36)×10-3ng/ml]显著减低,P<0.01,但仍未达正常水平[(2461±949)ng/ml,(135.42±27.46)×10-3ng/ml].临床研究Hp阳性CAG患者,血清NO(5834±1896)ng/ml、ET(91.18±34.19)×10-3ng/ml明显高于Hp阴性CAG[(2773±1896)ng/ml,(68.37±14.24)×10-3ng/ml],P<0.01,也高于Hp阳性CSG患者[(3420±1024)ng/ml,(68.90±19.47)×10-3ng/ml],P<0.01.结论:Hp相关CAG血中NO和ET水平显著升高,二者呈正相关,根除Hp后,NO和ET水平显著降低.

AIM:To investigate the changes of nitric oxide (NO) and endothelin(ET) in rats and patients with Helicobacter pylori associated chronic atrophic gastritis (CAG) before and after eradication,and to explore the possible mechanism of Helicobacter pylori associated CAG. METHODS:Helicobacter pylor associated CAG Wistar rat model was induced with sodium, eoxycholate, sodium salicylate, ethanol and culture broth of H.pylori which were orally administered. Model rats were randomly divided into three groups: Group A: Helicobacter pylori eradication with standard triple therapy for two weeks (Amoxicilline+ Timidazole + Denol); Group B: naturally restoring group, only given distilled water as placebo; Group C: the normal control. 3 months after treatment, all the rats were killed. The blood level of NO and ET was measured. 42 caes of Helicobacter pylori infected CAG patients,25 Helicobacter pylori uninfected CAG patients, and 21 Helicobacter pylori infected chronic superficial gastritis (CSG) patients were included in this study. The blood level of NO and ET was measured. RESULTS:The blood level of NO and ET was lower in Helicobacter pylori eradication group(3 672±1 845)ng/ml, (181.14 ± 22.5)× 10-3ng/ml than those in naturally restoring group (887±1 896)ng/ml, (211.67±34.36)×10-3ng/ml , P <0.01. The blood level of NO and ET was higher in Hp infected CAG (5 834±1 896) ng/ml,(91.18±34.19)×10-3ng/ml than those in Hp uninfected CAG (2 773 ± 1 896) ng/ml,(68.37 ± 14.24)× 10-3 ng/ml and infected CSG patients (3 420±1 024) ng/ml,(68.90±19.47)×10-3 ng/ml (P <0.01). CONCLUSION:Helicobacter pylori associated CAG is accom- panied by an enhanced serum NO and plasma ET. This may be one of the pathogenic mechanisms of Helicobacter pylori associated CAG.