Zhao Junke, Hao Suqi, Chen Yan, Ye Xiaoxing, Fang Pengchao, Hu Haiyan
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Colloids Surf B Biointerfaces. 2024 Apr;236:113798. doi: 10.1016/j.colsurfb.2024.113798. Epub 2024 Feb 12.
Ulcerative colitis (UC) is a chronic and progressive inflammatory disease that damages the colonic mucosa and disrupts the intestinal epithelial barrier. The current clinical treatment for UC is mainly chemotherapy, which has the limited effectiveness and severe side effects. It mainly focuses on the treatment of inflammation while neglecting the repair of the intestinal mucosa and the restoration of the microbiota balance. Here, we aimed to address these challenges by using an amphipathic bile acid -tauroursodeoxycholic acid (TUDCA) to replace cholesterol (CHL) in conventional liposomes. We prepared TUDCA/Emodin liposomes by incorporating the hydrophobic drug emodin. The experimental results indicated that TUDCA/Emodin Lip had uniform particle size distribution, good stability, low cytotoxicity, and exhibited good mucus permeability and anti-inflammatory activity in in vitro experiments, and was able to protect cells from oxidative stress. After oral administration, TUDCA/Emodin Lip significantly alleviated the severity of UC. This was evidenced by increased colon length, decreased inflammation and reduced colonic endoplasmic reticulum stress (ERS). Furthermore, TUDCA/Emodin Lip maintained the normal levels of the tight junction proteins Claudin-1 and ZO-1, thereby restoring the integrity of the intestinal barrier. Importantly, TUDCA/Emodin Lip also promoted the ecological restoration of the gut microbiota, increased overall abundance and diversity. Taken together, TUDCA/Emodin Lip can fundamentally restore intestinal homeostasis, this work provides a new, efficient and easily transformable treatment for UC.
溃疡性结肠炎(UC)是一种慢性进行性炎症性疾病,会损害结肠黏膜并破坏肠道上皮屏障。目前UC的临床治疗主要是化疗,其疗效有限且副作用严重。它主要侧重于炎症治疗,而忽视了肠黏膜的修复和微生物群平衡的恢复。在此,我们旨在通过使用两亲性胆汁酸——牛磺熊去氧胆酸(TUDCA)替代传统脂质体中的胆固醇(CHL)来应对这些挑战。我们通过包载疏水性药物大黄素制备了TUDCA/大黄素脂质体。实验结果表明,TUDCA/大黄素脂质体粒径分布均匀、稳定性好、细胞毒性低,在体外实验中表现出良好的黏液通透性和抗炎活性,并且能够保护细胞免受氧化应激。口服给药后,TUDCA/大黄素脂质体显著减轻了UC的严重程度。结肠长度增加、炎症减轻以及结肠内质网应激(ERS)降低证明了这一点。此外,TUDCA/大黄素脂质体维持了紧密连接蛋白Claudin-1和ZO-1的正常水平,从而恢复了肠道屏障的完整性。重要的是,TUDCA/大黄素脂质体还促进了肠道微生物群的生态恢复,增加了总体丰度和多样性。综上所述,TUDCA/大黄素脂质体可以从根本上恢复肠道稳态,这项工作为UC提供了一种新的、高效且易于转化的治疗方法。