Open Access

ARTICLE

Co-Encapsulation of Silymarin and Mesenchymal Stromal Cells in PEG Norbornene Microgels Enhances HepG2 Cell Resistance to Inflammatory Damage

Zhihuan Li^1,#, Shiqi Lei^1,#, Yajuan Guo¹, Renmeng Liu¹, Lei Yang¹, Yuheng Du¹, Xingdan Wang¹, Yun Zou^2,*, Kun Jiang^1,*, Zhongliang Jiang^1,*

1 School of Chemical Engineering, University of Science and Technology Liaoning, Anshan, China
2 Department of Stomatology, Ansteel General Hospital, Anshan, China

* Corresponding Authors: Yun Zou. Email: ; Kun Jiang. Email: ; Zhongliang Jiang. Email:
# These authors contributed equally to this work

(This article belongs to the Special Issue: Polymer Materials for Tissue Engineering and Cell Encapsulation)

Journal of Polymer Materials 2026, 43(2), 10 https://doi.org/10.32604/jpm.2026.081661

Received 06 March 2026; Accepted 03 June 2026; Issue published 30 June 2026

Abstract

Inflammatory liver injury represents a significant clinical challenge, characterized by a hostile immune microenvironment and extensive tissue damage. Although silymarin and mesenchymal stromal cells (MSCs) show promise in treating inflammatory liver injury, their efficacy is restricted by the drug’s poor bioavailability while MSC therapy is hampered by low cellular viability under inflammatory stress. To overcome these challenges, we engineered a droplet-microfluidic-assisted platform to co-encapsulate silymarin and MSCs within uniform, biocompatible polyethylene glycol-norbornene (PEGNB) hydrogel microspheres. This design establishes a dual-functional scaffold that supports MSC survival by shielding them from the harsh milieu while enabling the sustained, localized release of silymarin. Crucially, we elucidate a synergistic mechanism wherein the sustained release of silymarin modulates the local microenvironment, and augmenting the paracrine activity of the co-encapsulated MSCs. This synergy is significantly supported by a marked elevation in the expression of anti-inflammatory factors, including Interleukin-10 (IL-10) and Transforming Growth Factor-β (TGF-β). Establishing an indirect co-culture via transwell inserts, we demonstrate that this bio-functionalized platform significantly mitigates Lipopolysaccharide (LPS)-induced damage in HepG2 cells by suppressing pro-inflammatory cytokines, including Tumor Necrosis Factor-α (TNF-α) and Interleukin-6 (IL-6), while preserving hepatocyte metabolic stability against inflammatory stress. This high-throughput strategy offers a promising approach to modulate pathological stress microenvironments, driving advancements in precision regenerative medicine.

---

Keywords

---