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SCIE SCOPUS
Prednisone 투여에 의한 흰쥐 위점막 손상과 Liposomal Superoxide Dismutase 의 보호효과
The Development of Gastric Mucosal Injury in Predisone Treated Rats , and Protective Effect of Liposomal Superoxide Dismutase
백광진 , 이희성 ( Kwang Jin Baek , Hee Sung Lee )
BMB Reports 22권 2호 170-177(8pages)
UCI I410-ECN-0102-2008-470-002222262

In the stomach of rats treated with prednisone (10 ㎎/100 g body weight) or liposomal superoxide dismutase (3,000 units) followed by prednisone (10 ㎎/100 g body weight), changes of the activities of superoxide dismutase (EC 1.5.1.1, SOD), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7) and xanthine oxidase (1.1.3.22), as well as the macroscopical and microscopical changes within the gastric mucosa were investigated, and disc gel electrophoresis was used for confirmation of SOD in rat stomach. The results were summarized as follows: 1. In most of experimental groups, activities of Cu, Zn-SOD and catalase were higher than those in the controls. 2. In all experimental groups excepts 2nd day after the treatment of prednisone, the peroxidase activity showed lower than that in the controls (p$lt;0.01). 3. The activities of Cu, Zn-SOD, Mn-SOD, catalase and peroxidase in the liposomal SOD and prednisone treated groups appeared to be higher than those in the prednisone treated groups. 4. The activity of xanthine oxidase increased in the prednisone treated groups compared with the prednisone and liposomal SOD treated groups, and the activity showed higher in prednisone treated groups compared with the control value (p$lt;0.01). 5. Cu, Zn-SOD and Mn-SOD were confirmed by disc gel electrophoresis. 6. The gastric lesions (necrotic debris, mucosal and submucosal hemorrhage) occurred in the prednisone treated gorups, whereas, in the prednisone and liposomal SOD treated groups, the gastric mucosa were intact. From the above results, prednisone could enhance the activity of xanthine oxidase and results in gastric lesions, but the liposomal SOD may effectively protect the stomach from the development of gastric lesions. Accordingly, it could be suggested that the production of oxygen radicals (superoxide radical, hydroxyl radical, hydrogen peroxide and singlet oxygen) due to the increase of the activity of xanthine oxidase develop the gastric mucosal lesions. And SOD, catalase and peroxidase, scavengers of free radicals, may play an important role in the gastric mucosal defence mechanism.

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