L－SOD对DDC诱发大鼠急性胃粘膜损伤的保护作用

Protective effect of liposome-encapsulated SOD on acute gastric mucosal lesions in rats-induced by diethyldithiocarbamate

本实验通过皮下注射ＤＤＣ（二乙基二硫代氨基甲酸钠）诱发大鼠急性胃粘膜损伤（ＡＧ－ＭＬ）模型，观察脂质体携载ＳＯＤ（Ｌ－ＳＯＤ）对此损伤的保护作用。发现ＤＤＣ能剂量依赖地诱发ＡＧＭＬ。预先静脉注射Ｌ－ＳＯＤ（３００００Ｕ／ｋｇ），可使胃粘膜ＳＯＤ和ＧＳＨ－Ｐｘ活性受到保护，ＭＤＡ含量减少（Ｐ＜０．０５），胃粘膜血流量（ＧＭＢＦ）提高１２％，粘膜损伤指数下降６０％。表明ＤＤＣ能稳定诱发ＡＧＭＬ，Ｌ－ＳＯＤ对这种损伤具有保护作用，其机理与增强组织的抗氧化功能有关。Ｌ－ＳＯＤ可能具有临床应用价值。

A model of acute gastric mucosal lesion was induced by diethyldithiocarba-mate (DDC)and the protective effect of liposome-encapsulated SOD( L-SOD ) against thedamage was invastigated. The results showed that DDC induced lesions was in a dose-dependent manner. Pretreatment with L-SOD(30000U/kg,i.v ) would inhibit the decreaseof SOD and GSH-Px activities(6.66 ± 0.84 vs 4.32 ± 0.57 Nu/mg·pro, 32.24 ± 5.54 vs26.18 ± 2.24U/mg·pro·min￣(-1),P<0.01,P<0.05, respectively)effectively.It reduced the in-crease of MDA levels(1.08 ± 0.11 vs 1.21 ± 0.10 nmol/mg.pro,P<0.05),increased thegastric mucosal blood flow by 12%, and decreased the mucosal lesion index by 60%.Thepresent study demonstrated that DDC induced gastric mucosal lesions consistently,its me-chanism might be involved in lipid peroxident via the generation of oxygen free radicals.L-SOD would prevent DDC-induced gastric mucosal injury by augmenting SOD activity in gastric tissue and would have a clinical application.