Natural drug-derived carbon dots as a novel oral dosing strategy for gouty arthritis.

BACKGROUND

Gouty arthritis (GA), an acute inflammatory disorder triggered by monosodium urate (MSU) crystal deposition, poses a significant global health challenge due to rising prevalence and limitations of current therapies, including single-target mechanisms and adverse effects. The newly synthesized carbon dots (CDs) via high-temperature processing exhibit improved therapeutic efficacy and reduced toxicity.

METHODS

Aconitum Lateralis Radix Praeparata Carbonis-derived Carbon Dots (ALRPC-CDs) were synthesized through a high-temperature carbonization method (400 °C) and characterized by transmission electron microscopy (TEM), high-resolution TEM (HRTEM), ultraviolet-visible (UV-Vis) spectroscopy, fluorescence (FL) spectroscopy, Fourier-transform infrared (FTIR) spectroscopy, X-ray photoelectron spectroscopy (XPS), X-ray diffraction (XRD), and high-performance liquid chromatography (HPLC). Pharmacodynamic assessments included hot-plate analgesia tests, xylene-induced ear edema assays, monosodium urate (MSU)-induced gouty arthritis models, and oxonate potassium/hypoxanthine-induced hyperuricemic models. Biocompatibility was systematically evaluated in LO2 hepatocytes and 293 T renal cells using cell counting kit-8 (CCK-8) assays.

RESULTS

ALRPC-CDs exhibited monodisperse spherical morphology (1.78 ± 0.42 nm) with graphitic lattice structures (d-spacing 0.212 nm), displaying excitation/emission maxima at 314/417 nm. Pharmacodynamic studies revealed their multi-mechanistic therapeutic effects, including robust suppression of the TLR2/4-MyD88-NF-κB pathway, inhibition of xanthine oxidase activity, and significant urate-lowering effects, alongside anti-inflammatory, analgesic, and anti-hyperuricemic activity comparable to clinical controls. Biocompatibility was confirmed with excellent safety profiles.

CONCLUSION

This study demonstrates that ALRPC-CDs alleviate gouty arthritis through dual suppression of inflammatory signaling (TLR2/4-MyD88-NF-κB) and uric acid metabolism (xanthine oxidase inhibition), bridging herbal medicine and nanotechnology for multi-target therapeutic development.