Mard Seyyed Ali, Veisi Ali, Ahangarpour Akram, Gharib-Naseri Mohammad Kazem
Physiology Research Center (PRC), Research Center for Infectious Diseases of Digestive System, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Physiology Research Center (PRC), Diabetes research center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
J Physiol Sci. 2015 Nov;65(6):545-54. doi: 10.1007/s12576-015-0392-5. Epub 2015 Aug 29.
It is well known that hydrogen sulfide (H2S) protects the gastric mucosa against gastric acid and other noxious stimulants by several mechanisms but until now the effect of gastric acid on H2S production has not been evaluated. This study was performed to determine the effect of basal and stimulated gastric acid secretion on mRNA and protein expression of cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS), and on mucosal release of H2S in rats. Seventy-two male rats were randomly assigned into 9 groups (8 in each)-control, distention, and pentagastrin-induced gastric acid secretion groups. The effects of 15% alcohol solution, propargylglycine (PAG), L-NAME, and pantoprazole were also investigated. Under anesthesia, animals underwent tracheostomy and midline laparotomy. A catheter was inserted into the stomach through the duodenum for gastric washout. At the end of the experiments, the animals were killed and the gastric mucosa was collected to measure H2S concentration and to quantify mRNA expression of CSE and CBS by quantitative real-time PCR, and expression of their proteins by western blot. Basal and stimulated gastric acid secretion increased mucosal levels of H2S, and mRNA and protein expression of CSE. Pantoprazole and L-NAME reversed H2S release and restored protein expression of CSE to the control level. Pantoprazole, but not propargylglycine, pretreatment inhibited the elevated level of protein expression of eNOS in response to distention-induced gastric acid secretion. Our findings indicated that NO mediated the stimulatory effect of gastric acid on H2S release and protein expression of CSE.
众所周知，硫化氢（H2S）通过多种机制保护胃黏膜免受胃酸和其他有害刺激，但迄今为止，胃酸对H2S产生的影响尚未得到评估。本研究旨在确定基础胃酸分泌和刺激胃酸分泌对大鼠胱硫醚γ-裂解酶（CSE）和胱硫醚β-合酶（CBS）的mRNA和蛋白表达以及胃黏膜H2S释放的影响。72只雄性大鼠被随机分为9组（每组8只）——对照组、扩张组和五肽胃泌素诱导的胃酸分泌组。还研究了15%乙醇溶液、炔丙基甘氨酸（PAG）、L-精氨酸甲酯（L-NAME）和泮托拉唑的作用。在麻醉下，动物进行气管切开术和中线剖腹术。通过十二指肠插入一根导管到胃中进行洗胃。实验结束时，处死动物并收集胃黏膜，以测量H2S浓度，并通过定量实时PCR定量CSE和CBS的mRNA表达，通过蛋白质印迹法定量其蛋白质表达。基础胃酸分泌和刺激胃酸分泌增加了胃黏膜H2S水平以及CSE的mRNA和蛋白表达。泮托拉唑和L-NAME逆转了H2S释放，并使CSE的蛋白表达恢复到对照水平。泮托拉唑预处理可抑制因扩张诱导的胃酸分泌而导致的内皮型一氧化氮合酶（eNOS）蛋白表达升高，但炔丙基甘氨酸预处理则无此作用。我们的研究结果表明，一氧化氮（NO）介导了胃酸对H2S释放和CSE蛋白表达的刺激作用。
