Surface-Mediated Immunomodulation by Electrostatic Immobilization of Naproxen on Plasma-Aminated Poly(ε-caprolactone) Films Rescues Osteogenic Differentiation via Attenuation of NF-κB Signaling
- 1Chonnam National University , , ,
- 2Chosun University , , ,
Abstract
Chronic inflammation following biomaterial implantation often leads to fibrous encapsulation and compromised osseointegration, particularly in clinically inflamed environments. We developed a surface-functionalized poly(ε-caprolactone) (PCL) platform to modulate the early inflammatory microenvironment via surface-mediated drug release. PCL films were aminated by plasma polymerization, enabling the electrostatic immobilization of naproxen. Surface characterization by zeta potential analysis, X-ray photoelectron spectroscopy (XPS), and atomic force microscopy (AFM) confirmed successful amine functionalization and subsequent naproxen loading. The functionalized films exhibited a pronounced early burst release of naproxen within the initial hours after immersion, addressing the early phase of post-surgical inflammation. In vitro studies using MC3T3-E1 pre-osteoblasts under lipopolysaccharide (LPS)-induced inflammatory conditions showed that naproxen released from the surface significantly reduced pro-inflammatory cytokine secretion, including IL-6 and IL-1β. The cytokine-suppressive effect of the naproxen-functionalized surface was further supported by mechanistic experiments showing that soluble naproxen attenuated LPS-induced NF-κB p65 phosphorylation and nuclear translocation. These results suggest that the anti-inflammatory response mediated by surface-released naproxen is, at least in part, attributable to the intrinsic NF-κB-modulating activity of naproxen. Modulation of the inflammatory microenvironment restored osteogenic differentiation, with increased expression of RUNX2, ALP, and OPN, and enhanced matrix mineralization, as confirmed by Alizarin Red S staining. These findings demonstrate that surface-mediated delivery of naproxen enables temporally controlled osteoimmunomodulation and supports osteogenic function under inflammatory stress, underscoring the potential of this surface-engineering strategy for bone-regenerative applications.
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BibTeX
@article{kim2026surfacemediated,
title = {{Surface-Mediated Immunomodulation by Electrostatic Immobilization of Naproxen on Plasma-Aminated Poly(ε-caprolactone) Films Rescues Osteogenic Differentiation via Attenuation of NF-κB Signaling}},
author = {Chang-Young Kim and Namuun Khentii and Ji-Hun Seok and Tien Ngoc Thuy Nguyen and Min-Suk Kook},
journal = {ACS omega},
year = {2026},
month = oct,
doi = {10.1021/acsomega.6c02070},
url = {https://europepmc.org/article/PMC/PMC13670297},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Surface-Mediated Immunomodulation by Electrostatic Immobilization of Naproxen on Plasma-Aminated Poly(ε-caprolactone) Films Rescues Osteogenic Differentiation via Attenuation of NF-κB Signaling
AU - Chang-Young Kim
AU - Namuun Khentii
AU - Ji-Hun Seok
AU - Tien Ngoc Thuy Nguyen
AU - Min-Suk Kook
PY - 2026
DA - 2026/10/01
JO - ACS omega
DO - 10.1021/acsomega.6c02070
UR - https://europepmc.org/article/PMC/PMC13670297
AB - Chronic inflammation following biomaterial implantation often leads to fibrous encapsulation and compromised osseointegration, particularly in clinically inflamed environments. We developed a surface-functionalized poly(ε-caprolactone) (PCL) platform to modulate the early inflammatory microenvironment via surface-mediated drug release. PCL films were aminated by plasma polymerization, enabling the electrostatic immobilization of naproxen. Surface characterization by zeta potential analysis, X-ray photoelectron spectroscopy (XPS), and atomic force microscopy (AFM) confirmed successful amine functionalization and subsequent naproxen loading. The functionalized films exhibited a pronounced early burst release of naproxen within the initial hours after immersion, addressing the early phase of post-surgical inflammation. In vitro studies using MC3T3-E1 pre-osteoblasts under lipopolysaccharide (LPS)-induced inflammatory conditions showed that naproxen released from the surface significantly reduced pro-inflammatory cytokine secretion, including IL-6 and IL-1β. The cytokine-suppressive effect of the naproxen-functionalized surface was further supported by mechanistic experiments showing that soluble naproxen attenuated LPS-induced NF-κB p65 phosphorylation and nuclear translocation. These results suggest that the anti-inflammatory response mediated by surface-released naproxen is, at least in part, attributable to the intrinsic NF-κB-modulating activity of naproxen. Modulation of the inflammatory microenvironment restored osteogenic differentiation, with increased expression of RUNX2, ALP, and OPN, and enhanced matrix mineralization, as confirmed by Alizarin Red S staining. These findings demonstrate that surface-mediated delivery of naproxen enables temporally controlled osteoimmunomodulation and supports osteogenic function under inflammatory stress, underscoring the potential of this surface-engineering strategy for bone-regenerative applications.
SN - 2470-1343
ER -