Department of Gastroenterology, 439, Hvidovre University Hospital , Kettegårds Alle 30, Hvidovre DK-2650, Denmark.
Am J Gastroenterol. 2010 Jul;105(7):1595-603. doi: 10.1038/ajg.2009.749. Epub 2010 Jan 19.
Impaired epithelial expression of peroxisome proliferator-activated receptor-gamma (PPARgamma) has been described in animal colitis models and briefly in patients with ulcerative colitis, but the functional significance in humans is not well defined. We examined PPARgamma expression and functional activity in human colonic epithelium and explored the potential of topical treatment with rosiglitazone (a PPARgamma ligand) in patients with ulcerative colitis.
Spontaneous and rosiglitazone-mediated PPARgamma and adipophillin expression (a gene transcriptionally activated by PPARgamma) were measured by reverse transcriptase PCR in colonic biopsies and isolated epithelial cells from patients with ulcerative colitis and controls. Fourteen patients with active distal ulcerative colitis were randomized to either rosiglitazone (4 mg) or mesalazine (1 g) enema treatment once daily for 14 days.
PPARgamma expression was fourfold reduced in epithelial cells from inflamed compared with uninflamed mucosa and controls. Adipophillin levels were decreased in parallel. Rosiglitazone induced a concentration-dependent increase in adipophillin levels and restored PPARgamma activity in epithelial cells from inflamed mucosa in vitro. Rosiglitazone enema treatment was well tolerated and reduced the Mayo ulcerative colitis score from 8.9 to 4.3 (P<0.01), similar to the effect of mesalazine. Rosiglitazone increased adipophillin levels in the epithelial cells of the patients, indicating PPARgamma activation in vivo.
Roziglitasone enemas improve impaired PPARgamma activity in inflamed colonic epithelium and have beneficial clinical effect in patients with active distal ulcerative colitis. These findings raise interest in further studies of PPARgamma ligands that exhibit their anti-inflammatory effect locally in the gut to avoid possible systemic side effects.
在动物结肠炎模型中以及在溃疡性结肠炎患者中简要地描述了过氧化物酶体增殖物激活受体-γ(PPARγ)的上皮细胞表达受损,但在人类中的功能意义尚不清楚。我们检测了人类结肠上皮细胞中的 PPARγ表达和功能活性,并探讨了在溃疡性结肠炎患者中局部使用罗格列酮(一种 PPARγ配体)治疗的潜力。
通过逆转录 PCR 测量溃疡性结肠炎患者和对照者的结肠活检和分离的上皮细胞中自发的和罗格列酮介导的 PPARγ和脂联素表达(一种受 PPARγ转录激活的基因)。将 14 例活动期远端溃疡性结肠炎患者随机分为罗格列酮(4 mg)或美沙拉嗪(1 g)灌肠治疗组,每日一次,共 14 天。
与非炎症性和对照粘膜相比,炎症性上皮细胞中的 PPARγ表达降低了四倍。脂联素水平也相应降低。罗格列酮在体外诱导脂联素水平的浓度依赖性增加,并恢复了炎症性粘膜上皮细胞中的 PPARγ活性。罗格列酮灌肠治疗耐受性良好,将 Mayo 溃疡性结肠炎评分从 8.9 降低至 4.3(P<0.01),与美沙拉嗪的效果相似。罗格列酮增加了患者上皮细胞中的脂联素水平,表明体内 PPARγ的激活。
罗格列酮灌肠可改善炎症性结肠上皮细胞中受损的 PPARγ活性,并对活动期远端溃疡性结肠炎患者具有有益的临床效果。这些发现引起了人们对进一步研究在肠道局部发挥抗炎作用而避免可能的全身副作用的 PPARγ配体的兴趣。