Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.
Department of Pharmaceutical Sciences, University of Michigan, Ann Arbor, Michigan 48109, United States.
ACS Nano. 2024 Feb 13;18(6):4704-4716. doi: 10.1021/acsnano.3c06107. Epub 2024 Jan 30.
Liver fibrosis is a life-threatening and irreversible disease. The fibrosis process is largely driven by hepatic stellate cells (HSCs), which undergo transdifferentiation from an inactivated state to an activated one during persistent liver damage. This activated state is responsible for collagen deposition in liver tissue and is accompanied by increased CD44 expression on the surfaces of HSCs and amplified intracellular oxidative stress, which contributes to the fibrosis process. To address this problem, we have developed a strategy that combines CD44-targeting of activated HSCs with an antioxidative approach. We developed hyaluronic acid-bilirubin nanoparticles (HABNs), composed of endogenous bilirubin, an antioxidant and anti-inflammatory bile acid, and hyaluronic acid, an endogenous CD44-targeting glycosaminoglycan biopolymer. Our findings demonstrate that intravenously administered HABNs effectively targeted the liver, particularly activated HSCs, in fibrotic mice with choline-deficient l-amino acid-defined high-fat diet (CD-HFD)-induced nonalcoholic steatohepatitis (NASH). HABNs were able to inhibit HSC activation and proliferation and collagen production. Furthermore, in a murine CD-HFD-induced NASH fibrosis model, intravenously administered HABNs showed potent fibrotic modulation activity. Our study suggests that HABNs have the potential to serve as a targeted anti-hepatic-fibrosis therapy by modulating activated HSCs via CD44-targeting and antioxidant strategies. This strategy could also be applied to various ROS-related diseases in which CD44-overexpressing cells play a pivotal role.
肝纤维化是一种危及生命且不可逆转的疾病。纤维化过程在很大程度上是由肝星状细胞(HSCs)驱动的,它们在持续的肝损伤过程中从静止状态向激活状态转化。这种激活状态负责肝组织中胶原蛋白的沉积,并伴随着 HSCs 表面 CD44 表达的增加和细胞内氧化应激的放大,这有助于纤维化过程。为了解决这个问题,我们开发了一种策略,将激活的 HSCs 的 CD44 靶向与抗氧化方法相结合。我们开发了透明质酸-胆红素纳米颗粒(HABNs),由内源性胆红素、抗氧化和抗炎胆汁酸和透明质酸组成,透明质酸是一种内源性 CD44 靶向糖胺聚糖生物聚合物。我们的研究结果表明,静脉给予 HABNs 可有效靶向肝,特别是纤维化小鼠中胆碱缺乏 l-氨基酸定义的高脂肪饮食(CD-HFD)诱导的非酒精性脂肪性肝炎(NASH)中的激活的 HSCs。HABNs 能够抑制 HSC 的激活、增殖和胶原产生。此外,在小鼠 CD-HFD 诱导的 NASH 纤维化模型中,静脉给予 HABNs 显示出强大的纤维化调节活性。我们的研究表明,HABNs 通过 CD44 靶向和抗氧化策略调节激活的 HSCs,具有作为靶向抗肝纤维化治疗的潜力。这种策略也可以应用于各种 ROS 相关疾病,其中 CD44 过表达的细胞起着关键作用。