大豆甙元磺酸钠对应激性胃粘膜损伤的影响及其机制探讨

目的：观察大豆甙元磺酸钠对力竭应激性渍疡的影响,探讨其可能的作用途径。方法：采用小鼠力竭性游泳,计数胃部溃疡点数建立应激溃疡模型,腹腔注射不同剂量的大豆甙元磺酸钠及一氧化氮合酶（NOS）抑制剂（L-NAME）并通过NADPH-黄递酶组织化学法检测胃壁NOS阳性神经元的变化。结果：大豆甙元磺酸钠具有保护胃粘膜的作用,且呈剂量效应;L-NAME可防止应激引起的胃粘膜损伤,L-NAME与有效剂量的大豆甙元磺酸钠联合使用后,大豆甙元磺酸钠对胃粘膜的保护作用明显增强;正常及应激小鼠胃壁NOS神经节数目基本不变,大豆甙元磺酸钠对正常小鼠胃壁NOS神经元影响不明显,而对应激小鼠胃壁单位面积及单个神经节内NOS阳性神经元数目均有显著降低作用。结论：应激时NO升高可导致溃疡,大豆甙元磺酸钠能够保护胃粘膜,其作用是通过抑制应激状态下NOS的升高,限制应激状态下NO过度升高,起到保护胃粘膜的作用。

Effects of sodium sulfonate daidzein on stress-induced gastric ulcer and its possible mechanism

Aim: To investigate the effects of sodium sulfonate daidzein(SSD) on stress-induced gastric ulcer and explore its possible mechanism.Methods: Using exhausted swimming and counting the number of gastric ulcer to establish the model of stress-induced gastric ulcer.Mouse experience intraperitoneal injection of different doses of SSD and L-NAME,and NDP histochemical method was used to detect the changes of nitric oxide synthase(NOS) positive neurons in stomach.Results: SSD had dose-dependent protective effect on gastric mucosa.L-NAME could prevent stress induced gastric lesion.After combined injection of L-NAME and effective dose of SSD,the protective effect of SSD on gastric mucosa was reinforced.The number of NOS ganglion was constant,and effective dose of SSD had slight effect on NOS-positive neurons in normal mouse while it decreased NOS positive neurons in per area and in per ganglia after stress.Conclusion: The increased nitric oxide(NO) leads to gastric ulcer during stress,SSD has protective effect on gastric mucosa and this effect may be mediated by inhibiting NOS and restricting the overproduction of NO during stress.