Zhang Zhe, Zou Yi-You, Zhou Yuan, Zhou Hui, Li Yuan-Jian
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China.
J Clin Gastroenterol. 2009 Mar;43(3):261-6. doi: 10.1097/MCG.0b013e3181624485.
Nitric oxide (NO) is a well-known gastric mucosa protection factor. Recently, it has been reported that methylated arginine compound such as asymmetric dimethylarginine (ADMA), which inhibits nitric oxide synthesis, may be related to the development of gastric mucosa injury in patients with Helicobacter pylori infection. In the present study, we tested the relationship between endogenous ADMA and gastric mucosa injury in H. pylor- infected patients and cultured gastric epithelial cells.
One hundred and fifty subjects with gastric diseases were entered in this study. The levels of ADMA in gastric juice and plasma were measured in both H. pylori+ and H. pylori- patients. We analyzed independent risk factors that contribute to ADMA levels by multiple linear regression analyses. Mucosal epithelium cells were treated with nicotine (10 microM) for 24 hours in the presence or absence of H. pylori. The concentrations of ADMA in the culture medium and the rate of cell apoptosis were determined.
The ADMA level in gastric juice was significantly increased in H. pylori+ patients (P<0.05), whereas there were no differences in the content of ADMA in the plasma between H. pylori+ patients and H. pylori- patients. Smoking and H. pylori infection were 2 independent risk factors contributing to ADMA levels, and in the population of H. pylori+ patients, the level of ADMA in smokers was higher compared with nonsmokers. Incubation of nicotine (10 microM) with epithelial cells for 24 hours further increased the elevated level of ADMA and the rate of cell apoptosis owing to H. pylori infection.
H. pylori infection caused an increase of ADMA levels in gastric juice, which was aggravated by smoking. Endogenous ADMA may be an important factor contributing to gastric mucosa injury.
一氧化氮（NO）是一种众所周知的胃黏膜保护因子。最近，有报道称抑制一氧化氮合成的甲基化精氨酸化合物，如不对称二甲基精氨酸（ADMA），可能与幽门螺杆菌感染患者胃黏膜损伤的发生有关。在本研究中，我们检测了幽门螺杆菌感染患者和培养的胃上皮细胞中内源性ADMA与胃黏膜损伤之间的关系。
150例胃病患者纳入本研究。检测幽门螺杆菌阳性和阴性患者胃液和血浆中的ADMA水平。我们通过多元线性回归分析分析了影响ADMA水平的独立危险因素。在有或无幽门螺杆菌存在的情况下，用尼古丁（10微摩尔）处理黏膜上皮细胞24小时。测定培养基中ADMA的浓度和细胞凋亡率。
幽门螺杆菌阳性患者胃液中的ADMA水平显著升高（P<0.05），而幽门螺杆菌阳性患者与阴性患者血浆中ADMA的含量没有差异。吸烟和幽门螺杆菌感染是导致ADMA水平升高的两个独立危险因素，在幽门螺杆菌阳性患者群体中，吸烟者的ADMA水平高于不吸烟者。尼古丁（10微摩尔）与上皮细胞孵育24小时进一步增加了因幽门螺杆菌感染而升高的ADMA水平和细胞凋亡率。
幽门螺杆菌感染导致胃液中ADMA水平升高，吸烟会加重这种情况。内源性ADMA可能是导致胃黏膜损伤的一个重要因素。
