Kim H, Kim K H
Department of Pharmacology and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea.
Dig Dis Sci. 1998 May;43(5):1042-9. doi: 10.1023/a:1018886919532.
The present study aimed to investigate the role of nitric oxide on the oxidative damage in isolated rabbit gastric cells exposed to hypoxia-reoxygenation. Nitric oxide synthesis modulators such as L-arginine and NG-nitro-L-arginine methyl ester, a nitric oxide donor, sodium nitroprusside, and superoxide dismutase were used to treat the cells, and the synthesis and secretion of mucus, lipid peroxide production, and glutathione contents of the cells were determined. As a result, hypoxia-reoxygenation decreased nitric oxide production and the synthesis and secretion of mucus, as well as glutathione contents of gastric cells, but hypoxia-reoxygenation increased lipid peroxide production. Pretreatment with L-arginine, a substrate for nitric oxide synthase, sodium nitroprusside, and superoxide dismutase prevented the increase in lipid peroxide production and the decreases in glutathione contents, as well as the synthesis and secretion of mucus induced by hypoxia-reoxygenation. However, NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, had no effect on these alterations. In conclusion, nitric oxide has an antioxidant defensive role on gastric cells by maintaining mucus and glutathione.
本研究旨在探讨一氧化氮在暴露于缺氧-复氧的离体兔胃细胞氧化损伤中的作用。使用一氧化氮合成调节剂如L-精氨酸和一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯、一氧化氮供体硝普钠以及超氧化物歧化酶处理细胞,并测定细胞黏液的合成与分泌、脂质过氧化物生成以及谷胱甘肽含量。结果显示,缺氧-复氧降低了一氧化氮生成、胃细胞黏液的合成与分泌以及谷胱甘肽含量,但增加了脂质过氧化物生成。用一氧化氮合酶的底物L-精氨酸、硝普钠和超氧化物歧化酶预处理可防止脂质过氧化物生成增加、谷胱甘肽含量降低以及缺氧-复氧诱导的黏液合成与分泌减少。然而,一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯对这些改变没有影响。总之,一氧化氮通过维持黏液和谷胱甘肽对胃细胞具有抗氧化防御作用。