摘要
AIM： To investigate the role of major non-protein and protein sulfhydryls and disulfides in chemically induced gastric hemorrhagic mucosal lesions （HML） and the mechanism of gastroprotective effect of sucralfate.METHODS： Rats were given 1 mL of 75% ethanol, 25%NaCl, 0.6 mol/L HCI, 0.2 mol/L NaOH or 1% ammonia solutions intragastrically （i.g.） and sacrificed 1, 3, 6 or 12 min later. Total （reduced and oxidized） glutathione （GSH ＋ GSSG）, glutathione disulfide （GSSG）, protein free sulfhydryls （PSH）, protein-glutathione mixed disulfides （PSSG） and protein cystine disulfides （PSSP） were measured in gastric mucosa and liver.RESULTS： Reduced glutathione （GSH） was depleted in the gastric mucosa after ethanol, HCI or NaCl exposure,while oxidized glutathione （GSSG） concentrations increased, except by HCI and NaOH exposure. Decreased levels of PSH after exposure to ethanol were observed,NaCl or NaOH while the total protein disulfides were increased. Ratios of reduced to oxidized glutathione or sulfhydrils to disulfides were decreased by all chemicals.No changes in thiol homeostasis were detected in the liver after i.g. abbreviation should be spelled out the first time here administration of ethanol. Sucralfate increased the concentrations of GSH and PSH and prevented the ethanol-induced changes in gastric mucosal thiol concentrations.CONCLUSION： Our modified methods are now suitable for direct measurements of major protein and nonprotein thiols/disulfides in the gastric mucosa or liver.A common element in the pathogenesis of chemically induced HML and in the mechanism of gastroprotective drugs seems to be the decreased ratios of reduced and oxidized glutathione as well as protein sulfhydryls and disulfides.
瞄准：在化学上导致的胃的出血性的粘膜损害(HML ) 和 sucralfate 的胃的保护的效果的机制调查主要非蛋白质和蛋白质 sulfhydryls 和二硫化物的角色。方法：老鼠 intragastrically 被给 75% 乙醇， 25% NaCl， 0.6 mol/L HCl， 0.2 mol/L NaOH 或 1% 氨溶液的 1 mL (i.g ) 并且牺牲了 1， 3， 6 或 12 min 以后。全部(减少并且氧化) 谷胱甘肽(GSH + GSSG ) ，谷胱甘肽二硫化物(GSSG ) ，蛋白质免费 sulfhydryls (PSH ) ，蛋白质谷胱甘肽混合了二硫化物(PSSG ) ，蛋白质胱氨酸二硫化物(PSSP ) 在胃粘膜和肝被测量。结果：当氧化谷胱甘肽(GSSG ) 集中增加了时，减少的谷胱甘肽(GSH ) 在乙醇， HCl 或 NaCl 暴露以后在胃粘膜被弄空，除了由 HCl 和 NaOH 暴露。在到乙醇的暴露以后的 PSH 的减少的层次被观察， NaCl 或 NaOH 当全部的蛋白质二硫化物被增加时。比率归结为氧化谷胱甘肽或到二硫化物的 sulfhydrils 被所有化学药品减少。在 i.g 缩写第一次应该这里被拼出以后，在巯基动态平衡的变化都没在肝被检测乙醇的管理。Sucralfate 增加了 GSH 和 PSH 的集中并且在胃的粘膜巯基集中阻止了导致乙醇的变化。结论：我们的修改方法现在在胃粘膜或肝对主要蛋白质和非蛋白质 thiols/disulfides 的直接大小合适。在化学上导致的 HML 的致病并且在胃的保护的药的机制的一个普通元素似乎是象蛋白质 sulfhydryls 和二硫化物一样的减少并且氧化的谷胱甘肽的减少的比率。
