Silymarin-Stabilized Gold Nanoparticles Combat Oxidative Stress in SH-SY5Y Cells
摘要
Neurodegenerative diseases present a growing clinical challenge, with oxidative stress playing a central role in neuronal damage and apoptosis. In this study, we synthesized silymarin-capped gold nanoparticles (SM-AuNPs) using an improved one-pot green method and report for the first time their antioxidant effects in a human neuronal cell model of oxidative stress-driven neurodegeneration. The nanoparticles were characterized using ultraviolet-visible (UV-Vis) spectroscopy, dynamic light scattering, Fourier transform-infrared spectroscopy (FT-IR), scanning transmission electron microscopy (STEM), and energy-dispersive X-ray spectroscopy (EDX). SM-AuNPs displayed a UV-Vis absorbance at 526 nm and exhibited a stable hydrodynamic diameter of 26.15 ± 0.43 nm, polydispersity index (0.125 ± 0.003), and zeta potential (− 42.7 mV) for 9 months. STEM analysis confirmed spherical morphology and size uniformity. EDX detected both gold and organic elements, and FT-IR analysis supported the reduction and capping of gold ions by SM. In vitro WST-1 assays using SH-SY5Y cells demonstrated that SM-AuNPs are biocompatible. Additionally, at 100 µg/mL, SM-AuNPs demonstrated significant antioxidant activity in the DPPH assay by reducing free radicals to 33.62%. This finding was corroborated by a cell-based DCF assay where 100 µg/mL SM-AuNPs reduced intracellular reactive oxygen species (ROS) by 64.19% (p < 0.0001) when administered as a prophylactic measure. When administered as a treatment, the same concentration reduced ROS by 38.88% (p < 0.0001). In all experiments, SM-AuNPs were either more effective than or comparable to free SM, AuNPs, and the positive controls. Our findings confirm the successful synthesis and high biocompatibility of SM-AuNPs. The observed potent antioxidant activity in a human neuronal cell model supports phytochemical-assisted gold nanoparticle synthesis as a viable and sustainable therapeutic approach for mitigating oxidative stress implicated in neurodegenerative diseases.