AIM： To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress （WRS） in rats.METHODS： WRS model of Sprague-Dawley （SD） rats was estab...AIM： To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress （WRS） in rats.METHODS： WRS model of Sprague-Dawley （SD） rats was established. Fifty-six male SD rats were randomly divided into control group, stress group and post-stress group. The stress group was divided into 1, 2 and 4 h stress subgroups. The post-stress group was divided into 24, 48 and 72 h subgroups. The pH value of gastric juice, ulcer index （UI） of gastric mucosa and H^＋, K^＋- ATPase activity of gastric parietal cells were measured. Ultrastructural change of parietal cells was observed under transmission electron microscope （TEM）.RESULTS： The pH value of gastric juice decreased time-dependently in stress group and increased in post-stress group. The H^＋, K^＋-ATPase activity of gastric parietal cells and the UI of gastric mucosa increased time-dependently in stress group and decreased in poststress group. Compared to control group, the pH value decreased remarkably （P = 0.0001）, the UI and H^＋, K^＋- ATPase activity increased significantly （P = 0.0001, P = 0.0174） in 4 h stress subgroup. UI was positively related with stress time （r = 0.9876, P 〈 0.01） but negatively with pH value （r = -0.8724, P 〈 0.05）. The parietal cells became active in stress group, especially in 4 h stress subgroup, in which plenty of intracellular canalicular and mitochondria were observed under TEM. In post-stress group, the parietal cells recovered to resting state.CONCOUSION： The acid secretion of parietal cells is consistent with their ultrastructural changes during the development and healing of stress ulcer induced by WRS and the degree of gastric mucosal lesions, suggesting gastric acid play an important role in the development of stress ulcer and is closely related with the recovery of gastric mucosal lesions induced by WRS.展开更多
AIM： To study the protective effect of a natural antioxidant, melatonin, against multistress condition induced lipid peroxidation v/a determination of gastric damage and plasma malondialdehyde （MDA） level by high p...AIM： To study the protective effect of a natural antioxidant, melatonin, against multistress condition induced lipid peroxidation v/a determination of gastric damage and plasma malondialdehyde （MDA） level by high performance liquid chromatography in rats. METHODS： We compared indomethacin-induced gastric damage and MDA plasma level in three groups of rats： unoperated, bile duct ligated and sham-operated and evaluated the role of the melatonin on gastric damage and plasma MDA level. Indomethacin and melatonin were injected intraperitoneally in doses of 50 mg/kg and 20 mg/kg, respectively. Animals were killed 4 h after indomethacin injection. RESULTS： Indomethacin induced more severe gastric damage and plasma MDA level in bile duct ligated animals was significantly higher （3.1±0.04 μmol/L） than sham （2.8±0.04 μmol/L） and unoperated animals （1.4±0.08 μmol/L）. Pretreatment with melatonin reduced indomethacin-induced gastric damage and plasma MDA level. CONCLUSION： Considering the results of this study, we suggest that in multistress conditions the intensity of gastric damage and the plasma MDA level are great and melatonin reduces the negative effect of lipid peroxidation and cell damage by oxidative stress in multistress conditions due to its antioxidizing activity.展开更多
目的观察电针足三里对应激性胃溃疡大鼠胃组织中热休克蛋白70(Heat Shock Protein 70,HSP70)m RNA表达的影响,探讨电针足三里防治胃溃疡的分子机制。方法将51只SD大鼠随机分为正常对照组(正常组)、应激性胃溃疡组(模型组)和电针足三里组...目的观察电针足三里对应激性胃溃疡大鼠胃组织中热休克蛋白70(Heat Shock Protein 70,HSP70)m RNA表达的影响,探讨电针足三里防治胃溃疡的分子机制。方法将51只SD大鼠随机分为正常对照组(正常组)、应激性胃溃疡组(模型组)和电针足三里组(电针组)。采用冷-束缚法制作应激性胃溃疡模型。造模后次日起电针组每天电针足三里20 min,连续3 d,左右足三里穴交替进行;模型组只进行与电针组一样的固定处理;正常组不做任何处理。按GUTH’s法计算胃黏膜损伤指数(Ulcer Index,UI)、HE染色法观察胃组织病理形态、RT-PCR法检测胃组织HSP70 m RNA表达。结果模型组与正常组比较,胃黏膜上可见数量、大小不等的明显溃疡,UI显著升高(P<0.001),HSP70 m RNA表达显著降低(P<0.05);电针组与模型组比较,胃组织病理变化有所改善,胃黏膜UI显著降低(P<0.05),HSP70 m RNA表达显著升高(P<0.01)。结论电针足三里可以上调应激性胃溃疡大鼠胃组织HSP70 m RNA表达,促进胃黏膜损伤的修复。展开更多
基金Supported by the Key Project of Military Medicine during the 10th five-year Plan period, PLA, China, No. 01Z059
文摘AIM： To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress （WRS） in rats.METHODS： WRS model of Sprague-Dawley （SD） rats was established. Fifty-six male SD rats were randomly divided into control group, stress group and post-stress group. The stress group was divided into 1, 2 and 4 h stress subgroups. The post-stress group was divided into 24, 48 and 72 h subgroups. The pH value of gastric juice, ulcer index （UI） of gastric mucosa and H^＋, K^＋- ATPase activity of gastric parietal cells were measured. Ultrastructural change of parietal cells was observed under transmission electron microscope （TEM）.RESULTS： The pH value of gastric juice decreased time-dependently in stress group and increased in post-stress group. The H^＋, K^＋-ATPase activity of gastric parietal cells and the UI of gastric mucosa increased time-dependently in stress group and decreased in poststress group. Compared to control group, the pH value decreased remarkably （P = 0.0001）, the UI and H^＋, K^＋- ATPase activity increased significantly （P = 0.0001, P = 0.0174） in 4 h stress subgroup. UI was positively related with stress time （r = 0.9876, P 〈 0.01） but negatively with pH value （r = -0.8724, P 〈 0.05）. The parietal cells became active in stress group, especially in 4 h stress subgroup, in which plenty of intracellular canalicular and mitochondria were observed under TEM. In post-stress group, the parietal cells recovered to resting state.CONCOUSION： The acid secretion of parietal cells is consistent with their ultrastructural changes during the development and healing of stress ulcer induced by WRS and the degree of gastric mucosal lesions, suggesting gastric acid play an important role in the development of stress ulcer and is closely related with the recovery of gastric mucosal lesions induced by WRS.
文摘AIM： To study the protective effect of a natural antioxidant, melatonin, against multistress condition induced lipid peroxidation v/a determination of gastric damage and plasma malondialdehyde （MDA） level by high performance liquid chromatography in rats. METHODS： We compared indomethacin-induced gastric damage and MDA plasma level in three groups of rats： unoperated, bile duct ligated and sham-operated and evaluated the role of the melatonin on gastric damage and plasma MDA level. Indomethacin and melatonin were injected intraperitoneally in doses of 50 mg/kg and 20 mg/kg, respectively. Animals were killed 4 h after indomethacin injection. RESULTS： Indomethacin induced more severe gastric damage and plasma MDA level in bile duct ligated animals was significantly higher （3.1±0.04 μmol/L） than sham （2.8±0.04 μmol/L） and unoperated animals （1.4±0.08 μmol/L）. Pretreatment with melatonin reduced indomethacin-induced gastric damage and plasma MDA level. CONCLUSION： Considering the results of this study, we suggest that in multistress conditions the intensity of gastric damage and the plasma MDA level are great and melatonin reduces the negative effect of lipid peroxidation and cell damage by oxidative stress in multistress conditions due to its antioxidizing activity.
文摘目的观察电针足三里对应激性胃溃疡大鼠胃组织中热休克蛋白70(Heat Shock Protein 70,HSP70)m RNA表达的影响,探讨电针足三里防治胃溃疡的分子机制。方法将51只SD大鼠随机分为正常对照组(正常组)、应激性胃溃疡组(模型组)和电针足三里组(电针组)。采用冷-束缚法制作应激性胃溃疡模型。造模后次日起电针组每天电针足三里20 min,连续3 d,左右足三里穴交替进行;模型组只进行与电针组一样的固定处理;正常组不做任何处理。按GUTH’s法计算胃黏膜损伤指数(Ulcer Index,UI)、HE染色法观察胃组织病理形态、RT-PCR法检测胃组织HSP70 m RNA表达。结果模型组与正常组比较,胃黏膜上可见数量、大小不等的明显溃疡,UI显著升高(P<0.001),HSP70 m RNA表达显著降低(P<0.05);电针组与模型组比较,胃组织病理变化有所改善,胃黏膜UI显著降低(P<0.05),HSP70 m RNA表达显著升高(P<0.01)。结论电针足三里可以上调应激性胃溃疡大鼠胃组织HSP70 m RNA表达,促进胃黏膜损伤的修复。
文摘一氧化氮(nitric oxide,NO)是一种由血管内皮细胞分泌的扩血管小分子活性物质,在血管扩张、局部组织灌注微循环的调节中发挥重要作用.应激性溃疡(stress ulcer,SU)是临床危重疾病、严重创伤等的常见严重并发症,确切机制尚不清楚.但近年来研究表明,局部胃粘膜血流量(gastricmucosal blood flow,GMBF)减少是主要的病理生理过程.我们通过观察 L-精氨酸、L-硝基-精氨酸甲酯(Nω-nitro-L-arginine methyl ester,L-NAME)对大鼠 SU 的影响,以探讨 NO在 SU 中的作用机制,为临床防治 SU 提供理论指导.
