Panax notoginseng-Derived Carbon Quantum Dots as a Novel Administration Strategy for Cerebral Ischemia-Reperfusion Injury Therapy

The present study aimed to synthesize Panax notoginseng-derived carbon quantum dots (PN-CDs) and explore their role in cerebral ischemia-reperfusion injury (CIRI). PN-CDs were synthesized by the hydrothermal method, and characterization and biocompatibility were assessed. Next, CIRI models were established using SH-SY5Y cells, primary neurons were treated with oxygen-glucose deprivation/reoxygenation (OGD/R), and rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R). After PN-CDs treatment, inflammation, apoptosis, and oxidative stress were detected in neuronal cells and rats using enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, flow cytometry, Western blot, and 2',7'-dichlorodihydrofluorescein diacetate probe. Meanwhile, 2,3,5-triphenyltetrazolium chloride, terminal deoxynucleotidyl transferase dUTP nick end labeling, Nissl, and hematoxylin and eosin staining were employed to measure the pathological damage of rats. Additionally, CIRI rats were administered with PN-CDs, Panax notoginseng saponins (PNS), Panax notoginseng (PN), or edaravone to investigate whether PN-CDs had the best effect. The findings revealed that PN-CDs exhibited favorable biocompatibility and crossed the blood-brain barrier. In vitro, PN-CD treatment inhibited oxidative stress, apoptosis, and inflammation, as evidenced by the decrease of interleukin-1β (IL-1β), IL-6, Bax, C-caspase-3, tumor necrosis factor-α, malondialdehyde, and reactive oxygen species and the increase of superoxide dismutase, Bcl-2, and glutathione. In CIRI rats, PN-CDs improved pathological damage and suppressed inflammation, apoptosis, and oxidative stress. The therapeutic effect of PN-CDs on CIRI was distinctly better than that of PNS and PN, and comparable to that of the first-line drug edaravone. In short, PN-CDs, a novel and efficient administration strategy, alleviates CIRI by inhibiting apoptosis, oxidative stress, and inflammation.