Uno Satoshi, Kawase Atsushi, Tsuji Akiko, Tanino Tadatoshi, Iwaki Masahiro
Department of Pharmacy, Kinki University, Osaka, Japan.
Drug Metab Pharmacokinet. 2007 Aug;22(4):313-21. doi: 10.2133/dmpk.22.313.
Adjuvant-induced arthritis (AA) rats have been used as an animal model for rheumatoid arthritis. Several studies have shown that the pharmacokinetics of a number of drugs are altered in AA rats. We investigated the effects of AA on the barrier functions of the intestine using a rat model. Intestinal CYP3A activities (midazolam 1'-hydroxylation and 7-benzyloxy-4-(trifluoromethyl)-coumarin 7-hydroxylation) in AA rats were significantly decreased compared with those in normal rats, with marked decrease observed in the upper segment of intestine. Intestinal P-glycoprotein (P-gp) activity at upper segment was also significantly decreased in AA rats to 60% of that in normal rats, and the other segments (middle and lower) of intestine also exhibited tendencies toward decrease in P-gp activity. This decrease was supported by the finding that levels of mdr1a mRNA and P-gp protein were decreased in AA rats. No significant differences were observed in intestinal paracellular and transcellular permeability between AA and normal rats. These results suggest that intestinal CYP3A and P-gp activities are decreased in AA rats, and that the pharmacokinetics and bioavailabilities of drugs whose membrane permeation is limited by intestinal CYP3A and/or P-gp may be altered in rheumatic diseases.
佐剂性关节炎(AA)大鼠已被用作类风湿性关节炎的动物模型。多项研究表明,AA大鼠体内多种药物的药代动力学发生了改变。我们使用大鼠模型研究了AA对肠道屏障功能的影响。与正常大鼠相比,AA大鼠的肠道CYP3A活性(咪达唑仑1'-羟化和7-苄氧基-4-(三氟甲基)-香豆素7-羟化)显著降低,在肠道上段观察到明显下降。AA大鼠上段肠道P-糖蛋白(P-gp)活性也显著降低至正常大鼠的60%,肠道其他段(中段和下段)的P-gp活性也有下降趋势。AA大鼠mdr1a mRNA和P-gp蛋白水平降低的发现支持了这种下降。AA大鼠和正常大鼠之间的肠道细胞旁和跨细胞通透性未观察到显著差异。这些结果表明,AA大鼠的肠道CYP3A和P-gp活性降低,并且在风湿性疾病中,其膜渗透受肠道CYP3A和/或P-gp限制的药物的药代动力学和生物利用度可能会改变。