Antioxidative Hyaluronic Acid-Bilirubin Nanomedicine Targeting Activated Hepatic Stellate Cells for Anti-Hepatic-Fibrosis Therapy.

Activated hepatic stellate cells Anti-liver-fibrosis therapy Antioxidative therapy Bilirubin Hyaluronic acid NASH Nanomedicine Nonalcoholic steatohepatitis

Journal

ACS nano
ISSN: 1936-086X
Titre abrégé: ACS Nano
Pays: United States
ID NLM: 101313589

Informations de publication

Date de publication:
30 Jan 2024
Historique:
medline: 30 1 2024
pubmed: 30 1 2024
entrez: 30 1 2024
Statut: aheadofprint

Résumé

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.

Identifiants

pubmed: 38288705
doi: 10.1021/acsnano.3c06107
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

Jongyoon Shinn (J)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Seojeong Park (S)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Seonju Lee (S)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Nayoon Park (N)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Seojeong Kim (S)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Seohui Hwang (S)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

James J Moon (JJ)

Department of Pharmaceutical Sciences, University of Michigan, Ann Arbor, Michigan 48109, United States.
Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109, United States.
Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan 48109, United States.
Department of Chemical Engineering, University of Michigan, Ann Arbor, Michigan 48109, United States.

Youngjoo Kwon (Y)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Yonghyun Lee (Y)

Department of Pharmacy, College of Pharmacy, Ewha Womans University, Seoul 03760, South Korea.

Classifications MeSH