...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Superoxide dismutase ameliorates TNBS-induced colitis by reducing oxidative stress, adhesion molecule expression, and leukocyte recruitment into the inflamed intestine
【24h】

Superoxide dismutase ameliorates TNBS-induced colitis by reducing oxidative stress, adhesion molecule expression, and leukocyte recruitment into the inflamed intestine

机译：超氧化物歧化酶通过减少氧化应激，黏附分子表达和白细胞募集进入发炎的肠道来改善TNBS诱导的结肠炎

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Oxidant stress has been implicated in the pathogenesis of inflammatory bowel disease. Antioxidant enzymes, such as superoxide dismutase (SOD), are candidate drugs for modulating this pathogenic factor. This study was designed to determine the therapeutic value of SOD in an experimental model of colitis and to study the mechanisms underlying its effects on intestinal inflammation. For that purpose, colitic (trinitrobenzene sulfonic acid-induced) and control rats were studied. Groups of colitic animals were treated with different doses of SOD (1, 4, or 13 mg/kg/day) or vehicle, starting after induction of colitis and during 7 days. Clinical and pathological markers of colitis severity and lipid peroxidation in colonic tissue were measured. Leukocyte-endothelial cell interactions in colonic venules and expression of vascular cell adhesion molecule 1 (VCAM-1) were determined. Development of colitis was associated with a significant loss in body weight, an increase in macroscopic and microscopic damage scores, and colonic myeloperoxidase activity. Administration of SOD significantly attenuated these changes in a dose-dependent manner and reduced lipid peroxidation in colonic tissue. The increase in leukocyte rolling and adhesion in colonic venules of colitic rats were significantly reduced by administration of SOD, 13 mg/kg/day. Development of colitis was associated with a marked increase in endothelial VCAM-1 expression, which was significantly reduced by treatment with SOD. In conclusion, treatment with SOD significantly reduces peroxidation reactions in the inflamed colon and affords significant amelioration of colonic inflammatory changes in experimental colitis. This effect is related to a reduction in VCAM-1 expression and leukocyte recruitment into the inflamed intestine.
机译：氧化应激与炎症性肠病的发病机理有关。抗氧化剂酶，例如超氧化物歧化酶（SOD），是调节这种致病因子的候选药物。这项研究旨在确定SOD在结肠炎实验模型中的治疗价值，并研究其对肠道炎症的潜在作用机制。为此目的，研究了结肠炎（三硝基苯磺酸诱导的）和对照大鼠。在诱发结肠炎后开始并在7天内，用不同剂量的SOD（1、4、13 mg / kg /天）或溶媒治疗了几组大肠动物。测量结肠组织中结肠炎严重程度和脂质过氧化的临床和病理学指标。测定结肠小静脉中的白细胞-内皮细胞相互作用和血管细胞粘附分子1（VCAM-1）的表达。结肠炎的发展与体重的显着降低，宏观和微观损伤评分的增加以及结肠髓过氧化物酶活性有关。 SOD的给药以剂量依赖性方式显着减弱了这些变化，并减少了结肠组织中的脂质过氧化作用。通过以13 mg / kg / day的SOD剂量给药，可显着降低结肠炎大鼠结肠小静脉白细胞滚动和粘附的增加。结肠炎的发生与内皮VCAM-1表达的显着增加有关，而SOD处理可明显降低该表达。总之，用SOD处理可显着减少发炎结肠中的过氧化反应，并显着改善实验性结肠炎中结肠炎性变化。该作用与VCAM-1表达的减少和白细胞募集入发炎的肠有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号