摘要
探讨内源性一氧化氮（NO）在大鼠应激性胃粘膜损伤中的作用及其与流基物质和脂质过氧化之间的关系。方法：建立冷束缚大鼠应激性胃粘膜损伤模型，观察：①内源性NO对胃粘膜损伤的影响；②应激后大鼠胃粘膜内巯基物质和脂质过氧化终产物丙二醛（MDA）含量的改变；③阻断NO对应激大鼠胃粘膜内上述两种物质含量的影响。结果：①外周给予NO阻断剂L－硝基精氨酸（L－NNA，12．5mg／kg）明显加重胃粘膜损伤；②应激导致胃粘膜内巯基物质含量显著降低，MDA含量明显增高；③但以L－NNA抑制内源性NO的生成，对应激大鼠胃粘膜上述两类物质的含量无明显影响。结论：内源性NO具有保护大鼠应激性胃粘膜损伤的作用，其保护作用似不通过内源性巯基物质的介导，也与胃粘膜脂质过氧化无关。
Objective: To investigate the effect of endogenous nitric oxide (NO) on gastic mucosal injury induced by stress and its relationship to sulfhydryl compounds and lipid peroxidation. Methods: After the gastric mucosal injury model induced by cold-restraint in rats was established, the present study was comleted by: ①observing the effect of endogenous NO on gastric mucosal damage, ②measuring the alterations of stressed gastric sulfhydryl compounds and malonaldehyde(MDA), the end product of lipid peroxidation, and ③evaluating the effect of inhibited NO on sulfhydryl compounds and MDA tissue levels of stressed gastric mucosa. Results: ①Pretreatment with the NO inhibitor, N-nitro-L-arginine (L-NNA. 12. 5 mg/kg),significantly intensified the gastric mucosal injury. ②After stress, the concentration of sulfhydryl compounds in the gastric mucosa was markedly decreased; MDA, however, was significantly increased. ③The inhibition of endogenous NO by L-NNA had no effect on the concentrations of both sulfhydryl compounds and MDA in gastric mucosa of stred rats. Conclusion: Endogenous NO could effectively protect the gastric mucosa from stress-induced damage in rats, and the protective role of NO is mediated neither by endogenous sulfhydryl compounds nor through lessening the extent of lipid peroxidation.
出处
《北京医科大学学报》
CSCD
1997年第6期510-512,共3页
Journal of Peking University(Health Sciences)
关键词
一氧化氮
药理学
应激性溃疡
胃粘膜损伤
Nitric oxide/pharmacol Gastric mucosa/drug eff Stress/pathol
