炎症性肠病患者结肠黏膜中白三烯B4代谢的改变。
Altered leukotriene B4 metabolism in colonic mucosa with inflammatory bowel disease.
作者信息
Ikehata A, Hiwatashi N, Kinouchi Y, Yamazaki H, Ito K, Toyota T
机构信息
Third Dept. of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
出版信息
Scand J Gastroenterol. 1995 Jan;30(1):44-9. doi: 10.3109/00365529509093234.
BACKGROUND
omega-Oxidation is regarded as the major pathway for leukotriene B4 (LTB4) metabolism. Very little is known about it in colonic mucosa with inflammatory bowel disease (IBD).
METHODS
We investigated the metabolic ratio of omega-oxidation to LTB4 biosynthesis in colonic mucosa from patients with IBD and control subjects. After incubation of colonic mucosa with 14C-arachidonic acid and ionophore A23187, we separated LTB4 and its omega-oxidative metabolites by high-performance liquid chromatography.
RESULTS
The rate of LTB4 omega-oxidation was comparable to the rate of its biosynthesis. The metabolic ratio was significantly decreased in inflamed mucosa with ulcerative colitis.
CONCLUSIONS
LTB4 omega-hydroxylase activity is an important factor in regulating LTB4 level in colonic mucosa, and the increased LTB4 level in inflamed mucosa with IBD, especially ulcerative colitis, is caused by decreased LTB4 omega-hydroxylase activity and increased 5-lipoxygenase activity.
背景
ω-氧化被认为是白三烯B4（LTB4）代谢的主要途径。在患有炎症性肠病（IBD）的结肠黏膜中，对此了解甚少。
方法
我们研究了IBD患者和对照受试者结肠黏膜中ω-氧化与LTB4生物合成的代谢比率。在用14C-花生四烯酸和离子载体A23187孵育结肠黏膜后，我们通过高效液相色谱法分离LTB4及其ω-氧化代谢产物。
结果
LTB4的ω-氧化速率与其生物合成速率相当。在溃疡性结肠炎的炎症黏膜中，代谢比率显著降低。
结论
LTB4 ω-羟化酶活性是调节结肠黏膜中LTB4水平的重要因素，IBD炎症黏膜尤其是溃疡性结肠炎中LTB4水平升高是由LTB4 ω-羟化酶活性降低和5-脂氧合酶活性增加所致。
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