活性氧、脂质过氧化及抗氧化剂在吲哚美辛诱导的大鼠胃黏膜损伤发病机制中的作用
Role of active oxygen, lipid peroxidation, and antioxidants in the pathogenesis of gastric mucosal injury induced by indomethacin in rats.
作者信息
Yoshikawa T, Naito Y, Kishi A, Tomii T, Kaneko T, Iinuma S, Ichikawa H, Yasuda M, Takahashi S, Kondo M
机构信息
First Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
出版信息
Gut. 1993 Jun;34(6):732-7. doi: 10.1136/gut.34.6.732.
The roles of active oxygen, lipid peroxidation, and the antioxidative defence mechanism in gastric mucosal injury induced by treatment with indomethacin in rats were investigated. The total area of gastric erosions and concentration of lipid peroxides in the gastric mucosa increased with time after administration of indomethacin (20 mg/kg, orally). The alpha-tocopherol:total cholesterol ratio in serum was significantly decreased and the activity of glutathione peroxidase, an important enzyme to scavenger of lipid peroxides, was inhibited by the administration of indomethacin. Treatments with superoxide dismutase and catalase inhibited the increases in gastric mucosal erosions and lipid peroxides in the gastric mucosa, and the reduction of serum alpha-tocopherol. Treatment with these scavengers did not improve the decreased glutathione peroxidase activity. These findings suggest that active oxygen species and lipid peroxidation play an important part in the pathogenesis of gastric mucosal injury induced by indomethacin, and that the decreased glutathione peroxidase activity aggravated the injury due to accelerated accumulation of hydrogen peroxide and lipid peroxides in the gastric mucosal cell.
研究了活性氧、脂质过氧化和抗氧化防御机制在吲哚美辛诱导的大鼠胃黏膜损伤中的作用。给予吲哚美辛（20mg/kg，口服）后，胃黏膜糜烂总面积和脂质过氧化物浓度随时间增加。血清中α-生育酚与总胆固醇的比值显著降低，脂质过氧化物清除剂的重要酶谷胱甘肽过氧化物酶的活性受到吲哚美辛给药的抑制。超氧化物歧化酶和过氧化氢酶处理可抑制胃黏膜糜烂和胃黏膜脂质过氧化物的增加以及血清α-生育酚的降低。这些清除剂处理并未改善降低的谷胱甘肽过氧化物酶活性。这些发现表明，活性氧和脂质过氧化在吲哚美辛诱导的胃黏膜损伤发病机制中起重要作用，并且谷胱甘肽过氧化物酶活性降低因胃黏膜细胞中过氧化氢和脂质过氧化物的加速积累而加重了损伤。
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